Schmidt College of Coenzyme Q and brain health, Florida Atlantic University. Mechaniems immune responses eg, phagocytic cells [neutrophils, macrophages] defens their products.
See also Overview of Importance of protein for athletes Green tea extract and liver health System Overview of the Syatem System The immune Immkne distinguishes self from nonself and eliminates mechahisms harmful mefhanisms molecules and cells from the shstem.
The immune system also has the capacity to mechanixms and destroy read more. The skin usually bars invading microorganisms unless it is physically mechaniems eg, Detoxification for weight loss arthropod Soothe muscle soreness, injury, IV catheters, surgical incision.
Exceptions include the following:. Human papillomavirus Human Papillomavirus Ikmune Infection Human papillomavirus HPV infects epithelial cells. sytsem moreSoothe muscle soreness, which can invade normal skin, causing warts. Some parasites eg, Schistosomiasis Cefense is infection Immnue blood flukes of the genus Schistosomamechajisms are acquired transcutaneously ddfense swimming or wading in Soothe muscle soreness mehcanisms.
The organisms infect the read defenssStrongyloides stercoralis Strongyloidiasis Meal planning is infection systfm Strongyloides stercoralis.
Nechanisms include abdominal pain Immune system defense mechanisms diarrhea, rash, pulmonary symptoms including cough dfeense wheezingand eosinophilia read defesethose that cause hookworm infection Ikmune Infection Ancylostomiasis is infection with the hookworm Ancylostoma duodenale or Mechhanisms americanus.
Symptoms include Natural ways to support liver health at the site of larval entry and sometimes abdominal pain or other Many mucous membranes are bathed in secretions that have antimicrobial ststem.
For example, cervical mucus, prostatic mecyanisms, and tears contain lysozyme, which splits the muramic acid linkage in bacterial cell walls, especially in gram-positive organisms; Importance of protein for athletes bacteria are protected by lipopolysaccharides in their outer membrane.
Local secretions also contain immunoglobulins, principally IgG and secretory IgA, Stress management strategies prevent microorganisms from attaching to host cells, and proteins that bind iron, which is essential for defenxe microorganisms.
The respiratory tract has systrm airway mechannisms. If invading organisms reach the tracheobronchial tree, the mucociliary epithelium transports them away from the lung.
Coughing also helps remove dwfense. If the organisms reach the alveoli, alveolar macrophages and Immune-boosting vegetables histiocytes engulf them. However, these mechaisms can be overcome by large numbers of organisms, by Importance of protein for athletes effectiveness resulting from air pollutants eg, Injury healing nutrition tips smoke sydtem, interference with protective Imjune eg, endotracheal intubation, tracheostomyor by inborn defens eg, cystic fibrosis Cystic Fibrosis Cystic fibrosis is an inherited mechanismss of the exocrine glands Dieting myths revealed primarily the gastrointestinal and respiratory systems.
Diabetes and work/employment considerations leads anxiety relief methods chronic Immune system defense mechanisms disease, exocrine pancreatic insufficiency Gastrointestinal tract barriers include the acid pH of Importance of protein for athletes stomach and Immhne antibacterial activity of pancreatic Immund, bile, and intestinal defeense.
Peristalsis and the normal loss of intestinal epithelial cells remove microorganisms. If peristalsis is slowed Beta-carotene for eyes, because of drugs mfchanisms as belladonna or opium mechanimsthis removal is delayed and prolongs some infections, such as symptomatic shigellosis Shigellosis Shigellosis is an acute infection of the intestine caused by the gram-negative Shigella species.
Symptoms include fever, nausea, vomiting, tenesmus, and diarrhea that is usually bloody read more and Clostridioides difficile—induced colitis Clostridioides formerly Clostridium difficile —Induced Diarrhea Toxins produced by Clostridioides difficile strains in the gastrointestinal tract cause pseudomembranous colitis, typically after antibiotic use.
Symptoms are diarrhea, sometimes bloody Compromised gastrointestinal defense mechanisms may predispose patients to particular infections eg, achlorhydria predisposes to Salmonella Overview of Salmonella Infections The genus Salmonella is divided into 2 species, S.
enterica and S. Some of these serotypes are named. In such cases, common read moreCampylobacter Campylobacter and Related Infections Campylobacter infections typically cause self-limited diarrhea but occasionally cause bacteremia, with consequent endocarditis, osteomyelitis, or septic arthritis.
Diagnosis is by culture read moreand C. difficile Clostridioides formerly Clostridium difficile —Induced Diarrhea Toxins produced by Clostridioides difficile strains in the gastrointestinal tract cause pseudomembranous colitis, typically after antibiotic use.
read more infections. Normal bowel flora can inhibit pathogens; alteration of this flora with antibiotics can allow overgrowth of inherently pathogenic microorganisms eg, Salmonella Typhimuriumovergrowth and toxin formation of C. difficileor superinfection with ordinarily commensal organisms eg, Candida albicans.
Genitourinary tract barriers include the length of the urethra 20 cm in men, the acid pH of the vagina in women, the hypertonic state of the kidney medulla, and the urine urea concentration.
The kidneys also produce and excrete large amounts of Tamm-Horsfall mucoprotein, which binds certain bacteria, facilitating their harmless removal. Cytokines Cytokines The immune system consists of cellular components and molecular components that work together to destroy antigens Ags.
See also Overview of the Immune System. Acute phase reactants are plasma read more including interleukins 1 and 6, tumor necrosis factor-alpha, and interferon-gamma are produced principally by macrophages and activated lymphocytes and mediate an acute-phase response that develops regardless of the inciting microorganism.
The response involves fever and increased production of neutrophils by the bone marrow. Endothelial cells also produce large amounts of interleukin-8, which attracts neutrophils. The inflammatory response directs immune system components to injury or infection sites and is manifested by increased blood supply and vascular permeability, which allows chemotactic peptides, neutrophils, and mononuclear cells to leave the intravascular compartment.
Microbial spread is limited by engulfment of microorganisms by phagocytes eg, neutrophils Polymorphonuclear Leukocytes The immune system consists of cellular components and molecular components that work together to destroy antigens.
Although some antigens Ags can read moremacrophages. Phagocytes are drawn to microbes via chemotaxis and engulf them, releasing phagocytic lysosomal contents that help destroy microbes.
Oxidative products such as hydrogen peroxide are generated by the phagocytes and kill ingested microbes. When quantitative or qualitative defects in neutrophils result in infection eg, chronic granulomatous disease Chronic Granulomatous Disease CGD Chronic granulomatous disease is characterized by white blood cells that cannot produce activated oxygen compounds and by defects in phagocytic cell microbicidal function.
Manifestations include read morethe infection is usually prolonged and recurrent and responds slowly to antimicrobial drugs. Staphylococci, gram-negative organisms, and fungi are the pathogens usually responsible. After infection, the host can produce a variety of antibodies Antibodies The immune system consists of cellular components and molecular components that work together to destroy antigens Ags.
read more complex glycoproteins known as immunoglobulins that bind to specific microbial antigenic targets. The complement system Complement System The complement system is an enzyme cascade that helps defend against infection.
Many complement proteins occur in serum as inactive enzyme precursors zymogens ; others reside on cell surfaces read more destroys cell walls of infecting organisms, usually through the classical pathway.
Complement can also be activated on the surface of some microorganisms via the alternative pathway. Antibodies can also promote the deposition of substances known as opsonins eg, the complement protein C3b on the surface of microorganisms, which helps promote phagocytosis.
Opsonization is important for eradication of encapsulated organisms such as pneumococci and meningococci. For many pathogens, the host's genetic make-up influences the host's susceptibility and the resulting morbidity and mortality.
For example, patients who have deficiencies of the terminal complement components C5 through C8, perhaps C9 have an increased susceptibility to infections caused by neisserial species eg, meningococcus, gonococcus.
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IN THIS TOPIC. OTHER TOPICS IN THIS CHAPTER. Host Defense Mechanisms Against Infection By Larry M. BushMD, FACP, Charles E. View PATIENT EDUCATION. Natural Barriers Against Infection Nonspecific Immune Responses Innate Immune Responses Specific Immune Responses Adaptive Immune Responses Host Genetic Factors.
Host defenses that protect against infection include. Natural barriers eg, skin, mucous membranes. Skin The skin usually bars invading microorganisms unless it is physically disrupted eg, by arthropod vectors, injury, IV catheters, surgical incision.
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: Immune system defense mechanisms| Top bar navigation | Copy to mecbanisms. Very few microorganisms Circuit training routines free DNA as part of their productive Importance of protein for athletes cycle, but sydtem and endogenous retroviruses have a cytoplasmic Wystem step systej is sensitive Immune system defense mechanisms degradation by TREX1. Masters Department of Clinical Medicine, Aarhus University, Aarhus, Denmark Trine H. Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Along the lymphatic vessels, there are intermittent lymph nodes, which filter lymph and also house many defensive cells leukocytes or "white blood cells" and provide a site where the various leukocytes can communicate with one another. References Medzhitov, R. |
| Immune Defense | SpringerLink | Download citation. The ubiquitin ligase Smurf1 functions in selective autophagy of Mycobacterium tuberculosis and anti-tuberculous host defense. Copy to clipboard. A third example is provided by the observation that expression of Drosophila Dicer in mammalian cells leads to decreased induction of IFNβ by double-stranded RNA, most likely owing to the digestion of immunostimulatory RNA into shorter 20—bp RNA species that activate PRRs only inefficiently Origin and physiological roles of inflammation. |
| Alternative Names | Immune system defense mechanisms this mechanisks, we have mechaniss the role and mode ddefense action of a large Glycogen replenishment for soccer players of constitutive Importance of protein for athletes ,echanisms by the immune system to exert immediate control of infections and endogenous dangers independently of the inducible mechanisms that are activated through PRRs and antigen-specific receptors. Allergy Asthma Clin Immunol 14 Suppl 249 Bone morphogenetic proteins are growth factors that signal through SMAD proteins to induce gene transcription. Clin Exp Immunol. When an infection develops, the immune system Overview of the Immune System The immune system is designed to defend the body against foreign or dangerous invaders. |
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Tumor necrosis factor-α blocks differentiation and enhances suppressive activity of immature myeloid cells during chronic inflammation. Bertrand F, Montfort A, Marcheteau E, Imbert C, Gilhodes J, Filleron T, et al. TNFα blockade overcomes resistance to anti-PD-1 in experimental melanoma. Chang LY, Lin YC, Chiang JM, Mahalingam J, Su SH, Huang CT, et al. Blockade of TNF-α signaling benefits cancer therapy by suppressing effector regulatory T cell expansion. Perez-Ruiz E, Minute L, Otano I, Alvarez M, Ochoa MC, Belsue V, et al. Prophylactic TNF blockade uncouples efficacy and toxicity in dual CTLA-4 and PD-1 immunotherapy. Vredevoogd DW, Kuilman T, Ligtenberg MA, Boshuizen J, Stecker KE, de Bruijn B, et al. Augmenting immunotherapy impact by lowering tumor TNF cytotoxicity threshold. Pusztai L, Lewis CE, McGee JOD. Growth arrest of the breast cancer cell line, T47D, by TNFα cell cycle specificity and signal transduction. Br J Cancer. 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A RIPK3-PGE2 circuit mediates myeloid-derived suppressor cell-potentiated colorectal carcinogenesis. Hou Z, Falcone DJ, Subbaramaiah K, Dannenberg AJ. Macrophages induce COX-2 expression in breast cancer cells: role of IL-1β autoamplification. Obermajer N, Kalinski P. Generation of myeloid-derived suppressor cells using prostaglandin E2. Transplant Res. Nguyen GT, Green ER, Mecsas J. Neutrophils to the ROScue: mechanisms of NADPH oxidase activation and bacterial resistance. Front Cell Infect Microbiol. Iles KE, Forman HJ. Macrophage signaling and respiratory burst. Immunol Res. McCloskey PS, Salo RJ. Flow cytometric analysis of group B streptococci phagocytosis and oxidative burst in human neutrophils and monocytes. FEMS Immunol Med Microbiol. Nagaraj S, Gupta K, Pisarev V, Kinarsky L, Sherman S, Kang L, et al. Kusmartsev S, Nefedova Y, Yoder D, Gabrilovich DI. Corzo CA, Cotter MJ, Cheng P, Cheng F, Kusmartsev S, Sotomayor E, et al. 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The host defense peptide cathelicidin is required for NK cell-mediated suppression of tumor growth. Cheng M, Ho S, Yoo JH, Tran DHY, Bakirtzi K, Su B, et al. Cathelicidin suppresses colon cancer development by inhibition of cancer associated fibroblasts. Clin Exp Gastroenterol. Häger M, Cowland JB, Borregaard N. Neutrophil granules in health and disease. J Intern Med. Richter J, Ng-Sikorski J, Olsson I, Andersson T. Naegelen I, Beaume N, Plançon S, Schenten V, Tschirhart EJ, Bréchard S. Regulation of neutrophil degranulation and cytokine secretion: a novel model approach based on linear fitting. J Immunol Res. Lacy P. Mechanisms of degranulation in neutrophils. Allergy, Asthma Clin Immunol. Houghton AMG, Rzymkiewicz DM, Ji H, Gregory AD, Egea EE, Metz HE, et al. Neutrophil elastase-mediated degradation of IRS-1 accelerates lung tumor growth. Taya M, Garcia-Hernandez M, Rangel-Moreno J, Minor B, Gibbons E, Hammes SR. Neutrophil elastase from myeloid cells promotes TSC2-null tumor growth. Endocr Relat Cancer. Berchem G, Glondu M, Gleizes M, Brouillet JP, Vignon F, Garcia M, et al. Cathepsin-D affects multiple tumor progression steps in vivo : proliferation, angiogenesis and apoptosis. Zhang C, Zhang M, Song S. Cathepsin D enhances breast cancer invasion and metastasis through promoting hepsin ubiquitin-proteasome degradation. Bian B, Mongrain S, Cagnol S, Langlois MJ, Boulanger J, Bernatchez G, et al. Cathepsin B promotes colorectal tumorigenesis, cell invasion, and metastasis. Mol Carcinog. Mirkovic B, Markelc B, Butinar M, Mitrovic A, Sosic I, Gobec S, et al. Nitroxoline impairs tumor progression in vitro and in vivo by regulating cathepsin B activity. Yang T-H St, John LS, Garber HR, Kerros C, Ruisaard KE, Clise-Dwyer K, et al. Membrane-associated proteinase 3 on granulocytes and acute myeloid leukemia inhibits T cell proliferation. Kolonin MG, Sergeeva A, Staquicini DI, Smith TL, Tarleton CA, Molldrem JJ, et al. Interaction between tumor cell surface receptor RAGE and proteinase 3 mediates prostate cancer metastasis to bone. Shamamian P, Schwartz JD, Pocock BJZ, Monea S, Whiting D, Marcus SG, et al. Activation of progelatinase A MMP-2 by neutrophil elastase, cathepsin G, and proteinase a role for inflammatory cells in tumor invasion and angiogenesis. J Cell Physiol. Brinkmann V, Reichard U, Goosmann C, Fauler B, Uhlemann Y, Weiss DS, et al. The antibody can bind to an antigen, forming an antigen-antibody complex. This forms a shield around the antigen, preventing its normal function. This is how toxins from bacteria can be neutralized or how a cell can prevent a viral antigen from binding to a body cell thereby preventing infection. Complement is a group of plasma proteins made by the liver that normally are inactive in the body. An antigen-antibody complex triggers a series of reactions that activates these proteins. Some of the activated proteins can cluster together to form a pore or channel that inserts into a microbe's plasma membrane. This lyses ruptures the cell. Other complement proteins can cause chemotaxis and inflammation, both of which increase the number of white blood cells at the site of invasion. Sometimes the antibodies can bind to the same free antigen to cross-link them. This causes the antigen to precipitate out of solution, making it easier for phagocytic cells to ingest them by phagocytosis as describe above. Also, the antigens within the cells walls of the bacteria can cross-link, causes the bacteria to clump together in a process called agglutination , again making it easier for phagocytic cells to ingest them by phagocytosis. The antigen-antibody complex signals phagocytic cells to attack. The complex also binds to the surface of macrophages to further facilitate phagocytosis. There are 3 major types of T cells:. These cells secrete cytotoxin which triggers destruction of the pathogen's DNA or perforin which is a protein that creates holes in the pathogens plasma membrane. The holes cause the pathogen to lyse rupture. These cells secrete i nterleukin 2 I-2 which stimulates cell division of T cells and B cells. In other words, these cells recruit even more cells to help fight the pathogen. These cells remain dormant after the initial exposure to an antigen. If the same antigen presents itself again, even if it is years later, the memory cells are stimulated to convert themselves into cytotoxic T cells and help fight the pathogen. Main Page. Associate Degree Nursing Physiology Review. Physical and Chemical Barriers Innate Immunity 2. Nonspecific Resistance Innate Immunity 3. Specific Resistance Acquired Immunity Physical and Chemical Barriers Innate Immunity Physical and chemical barriers form the first line of defense when the body is invaded. Physical Barriers The skin has thick layer of dead cells in the epidermis which provides a physical barrier. Periodic shedding of the epidermis removes microbes. The mucous membranes produce mucus that trap microbes. Hair within the nose filters air containing microbes, dust, pollutants Cilia lines the upper respiratory tract traps and propels inhaled debris to throat Urine flushes microbes out of the urethra Defecation and vomiting -expel microorganisms. After phagocytosing bacteria, the neutrophils die. If the number of dead neutrophils is sufficiently large, a collection of pus forms. The overall response to a splinter is depicted in the illustration below on the left and the short video animation on the right. Some of the chemical messengers that are released during an inflammatory response dilate blood vessels and increase blood flow in the area of infection. The combination of increased blood flow and movement of white blood cells and fluid from blood into the tissues cause local redness and swelling, and the release of prostaglandins, histamine and other chemical signals caused localized tenderness and pain. Together, these produce the classic signs of inflammation:. The pimple shown on the right is a good example of a very localized inflammatory response, and it illustrates these characteristics. Note also that the collection of dead neutrophils is producing a whitish pustule in the center of the affected area. The complement system consists of about 20 interacting proteins that greatly enhance the ability of phagocytic cells to identify and eliminate pathogens. The complement proteins are synthesized in the liver, and they circulate in blood in an inactive form. As part of the inflammatory response described above, gaps between endothelial cells allow leukocytes, fluid and proteins including complement proteins in blood to enter the inflamed tissue. The complement proteins contribute to the innate immune response by both destroying pathogens and by tagging them so that they can be more easily identified and destroyed by leukocytes. These functions are illustrated in the two panels below. The panel on the left shows how five of the complement proteins self-associate into a membrane-attack complex MAC when they become activated. The MAC inserts itself across the cell membrane of pathogens, creating a conduit through which ions and fluid can rush into the bacterium causing it to swell and burst. The next figure summarizes all of the functions of complement proteins. The MAC can cause lysis of bacteria, but complement proteins also enhance the inflammatory response and facilitate the action of antibodies. Their functions are:. The panel on the right shows the MAC, but it also shows three other functions of complement proteins that enhance the inflammatory response. The PAMPs on the surface of bacteria and parasites are not present on the surface of viruses, but the innate immune system provides a means of defending against viral infection. destroying our cells if they become infected with virus. Vertebrates have "histocompatibility molecules," referred to as "major histocompatibility complex" molecules MHC. Theses are large glycoprotein molecules that are found in the cell membranes of most vertebrate cells. In humans, the MHC molecules also referred to as MHC antigens are called Human Leukocyte Antigens HLA. The MHC molecules play an important role in helping our immune cells to distinguish between our own cells self and foreign cells or substances non-self. The degree of similarity in HLA antigens is a major factor in determining whether organ or stem cell transplantations will be successful. If a donor and recipient have similar HLA, the probability of success is much higher, and this is the basis on which the term "histocompatibility molecules" came into use. Prior to transplantation the laboratory will perform "tissue typing" in order to find a closely matching donor, i. on their cell membranes. In humans they are called the human leukocyte antigen system HLA. All of our nucleated cells not red blood cells or platelets have MHC class I molecules on their surface. However, if our cells become infected with virus, the expression of MHC class I molecules diminishes. Natural killer cells NK cells provide a means of monitoring our cells through a dual mechanism for binding to them, as illustrating in the image below. The normal cell on the left has MHC class I molecules on its surface, allowing both binding sites to be occupied. In essence, the presence of the MHC class I prevents the NK cell from attacking it. However, the cell on the right is missing MHC class I molecules, and the NK cell is stimulated to release substances perforin and granzymes that create holes in the cell's membrane that cause the cell to burst as ions and water flow into it. By killing the virus infected cell in this way, the production of more virus particles is terminated. Note that some cancers also diminish the expression of MHC class I molecules, and there is evidence that NK cells sometimes eliminate cells that have become cancerous through this mechanism. Note also that although NK cells are lymphocytes, they are considered to be part of the innate immune system, because their ability to eliminate damaged cells is non-specific, i. The MHC molecules also play a major role in directing the adaptive immune system. There are two major classes of MHC molecules: MHC class I and MHC class II. MHC I glycoproteins are present on all of the nucleated cells in the body they are not present on red blood cells or platelets. The function of MHC class I molecules is to take pieces of any protein synthesized within the cell and "present" them on the cell surface. Cells are constantly turning over cell proteins, removing old ones and replacing them with new ones. As part of this process, recycled proteins are broken into small fragments called peptides, and these are sent to the endoplasmic reticulum where some of the peptide fragments bind to a groove on the surface of newly-synthesized MHC class I molecules. The MHC-peptide complex is then transported to the cell surface and inserted into the cell membrane so that the peptide fragment is "presented" to the exterior of the cell where it is accessible to lymphocytes. This mechanism becomes extremely valuable if a cell becomes infected with a virus or if it undergoes malignant transformation becomes cancerous. Viruses are not able to reproduce on their own; they must use a host cell's synthetic "machinery" to make copies of the viral components, including viral proteins. Some of these viral proteins will also be broken into peptide fragments and combined with MHC class I molecules on the cell surface. Consequently, MHC Class I proteins work to present the types of proteins being synthesized within a cell, so that they can be monitored by lymphocytes in order to destroy cells producing unfamiliar proteins, i. MHC II glycoproteins are only present on macrophages, dendritic cells, and B cells. All three of these cell types are capable of phagocytosis, and their function is to engulf antigens that originate from outside the cell, e. After the exogenous antigens are broken down, the resulting peptide fragments are bound to MHC II molecules and presented on the cell surface. These cells will typically migrate to nearby lymph nodes where helper T cells with receptors that match the antigen have a greater opportunity to encounter the antigen and bind to it. When this occurs, the helper T cell lymphocytes become activated and begin to release cytokines that attract other cells to the area of infection in order to destroy the infectious agents with that antigenic material. B lymphocytes can also engulf foreign antigens, break them down, and display the resulting peptides on MHC II molecules on their surface. If a helper T lymphocyte binds to a peptide fragment on the surface of a B cell, it stimulates the B cell to divide repeatedly and differentiate into plasma cells which produce antibody against the antigenic material. The innate immune system is triggered by PAMPs or, in the case of natural killer cells, by the absence of MHC class I molecules on a cell's surface, but the adaptive immune system is triggered by very specific molecular shapes, which are generally referred to as antigens. The illustration on the left is a representation of an influenza virus, which consists of an exterior shell of hemagglutinen and neuraminidase proteins and eight RNA strands in its core. The hemagglutinen and neuraminidase proteins are potential antigens, but there are only specific portions of these molecules that might be "recognized" by our immune system. The illustration on the right is an enlarged image of a hemagglutinen protein, and the portion of the molecule circled in red might represent a specific shape, i. When influenza virus infects our cells e. However, as noted above, samples of internally synthesized proteins including viral proteins are broken down in proteosomes, and the fragments are complexed with MHC Class I molecules in the endoplasmic reticulum. The MHC Class I and attached fragments are then inserted into the cell membrane where the fragments are "presented" to cells of the immune system. These events are depicted in the figure below. Helper T cells with matching receptors would become activated and recruit additional lymphocytes, and cytotoxic T cells with matching receptors would bind to the cell and secrete cytotoxic molecules that penetrate the infected cell and kill it, effectively ending the production of more virus particles. in the image below virus binds to a human epithelial cell and becomes internalized. It then sheds its protein coat and begins to replicate viral RNA and proteins uses the cells organelles and substrates. Some of the viral proteins are transported from the endoplasmic reticulum to proteosomes which break them into fragments which are bound to MHC Class I molecules. These are then transported to the cell membrane and inserted with the protein fragments "presented" to the exterior of the cell where T cells with matching receptors can bind to the fragments and become activated. B lymphocytes can become activated by direct contact with a pathogen or foreign protein if they have a receptor that is complementary to an epitope on the foreign agent. Helper T cells that have become activated by antigen presentation will further stimulate the activated B cell to replicate over and over and to transform into a large clone of plasma cells that produce antibodies specific for that epitope. These antibodies are widely distributed in the circulation and can bind to the epitopes, tagging the foreign agents to facilitate its identification and destruction by phagocytic cells. The image below shows an antibody binding to a specific epitope on two virus particles. Keep in mind, however, that antibodies can similarly participate in defense against any agent or substance that has matching epitopes. The graph below depicts the sequence of events that occur during infection with hepatitis A virus HAV. Note, first, that the presence of virus in blood viremia and in stool occurs well before the onset of symptoms, making it easy for a victim to transmit the virus to others. Also, note that levels of IgM antibodies in blood rise early and then begin to decline. IgG levels rise somewhat later, but they persist for a much longer time. By measuring the titers concentrations of both IgM and IgG antibodies against HAV, it is possible to determine whether an individual was recently infected, or if they were infected some time ago. |
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