immunology
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immunology - Leaderboard
immunology - Details
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| 🇬🇧 | 🇬🇧 |
| How do these cells bind to antibodies, B-cells,T-cells? | B-cells by membrane bond antibodies or B-cell receptors (BCR), T-cells by T-cell receptors (TCR) |
| How do TCR and BCR recognize antibodies? | BCR (Ig) ands soluble antibodies recognize wide set of antigens by attachment , TCR recognize antibodies by antigen presenting cells that have that have peptides presented by MHC molecules . |
| What's a variable region V? | Antigen recognition |
| What's constant regions C? | Interaction with down stream signaling (telling lymphocytes to differentiate or die) molecules recreating antibodies that are triggered by antigens binding to BCR and TCR receptors . |
| What's the constant region recreating antibodies? | Interaction with receptors on phagocytes and complement proteins. |
| What are the types of antibodies of BCR (depending on their heavy chains)? | IgA(mucosal immunity ) , IgD( naive B-cell antigen receptor), IgE( defense against parasites), IgG(Opsonization),IgM(naive B-cell antigen). |
| What are the native B cells receptors ? | IgM and IgD |
| What's allelic exclusion ? | A process by which only one allele of a gene is expressed while the other allele is silenced. |
| What's affinity? | Interaction of one antibody-antigen region (Kd= 10-6, 10-9) |
| What's avidity? | Interaction of 2 or more antibody-antigen region, The measure of the total binding strength of an antibody is avidity,stronger as probability of repeated interaction. |
| What is the structure of T-cell receptors ? | 90% a and b chain,variable and constant regions variable regions recognize peptides presented on MHC.5-10% T-cells y and Ơ chains Recognize all kind of antigens do not require presentation on MHC.5% NK-T cells a and b chain variable regions do not show wide diversity, recognize lipid antigens presented by nonpolymorphic MHC . |
| What is positive and negative selection? | Positive selection of T-cells only the T-cells that recognize MHC molecules will survive, others will die. negative selection B and T cells those who recognize self antigens will die. |
| The differences in antigen recognition between BCR Ig and TCR genes? | They contain multiple variable regions (V) and one or few constant regions (C).Between V and C regions are several short diversity (D) and joining (J) segments.Only Ig heavy chain and TCR b-chain contain D segment. |
| What is the maturation and selection chain of B-lymphocytes? | Stem cell--> pro-B--> immature B--> mature B (follicular and memory) |
| What cells do not express Ig? | Stem cells and and pro B . |
| What cells move on to become pre B cells? | Only the cells that express the Igu heavy chain and other surrogate light chains survive and form the pre B cells. passing this check point releases survival signals.if the heavy chain is not made it will undergo apoptosis (cell death) . |
| What type of Ig are mature cells? | IgM and led they are mature B cells that can respond to antigens. |
| What is the maturation and selection chain of T-lymphocytes? | Stem cells --> pro T--> pre T--> double positive T-cells--> single positive T-cells |
| What are pro T cells? | Double negative T cells (CD4-, CD8-) that proliferate in response to IL7 In the thymus. If functional pre-TCR is not formed, cell will apoptose. |
| What are pre T cells? | In the thymus VDJ recombination takes place. TCR-b chains is expressed with invariant pre-Ta to form pre-TCR complex in pre-T cells. |
| What will pre-TCR will send signals to? | Inhibit apoptosis ,inhibit VDJ recombination in the homologous chromosome (allelic exclusion); stimulate TCR-a gene recombination. |
| How do pre-TCR cells survive? | If no functional TCR-a gene is expressed cells will die. Surviving cells express complete abTCR and CD8, CD4 receptors. which are called double-positive T cells. |
| What is Positive selection regarding T-cells? | Low affinity interaction between abTCR and MHC molecules sends survival signal. These cells may recognize complexes of microbial antigens bond to MHC with higher affinity. Cell that cannot recognize MHC molecules will die. Cells that recognize class I MHC will retain CD8, and cells that recognize class II MHC will retain CD4. this will generate single-positive T cells. |
| What is Negative selection regarding T-cells? | Double positive T cells that bind MHC with high affinity will die by apoptosis. This process eliminates lymphocytes that may react to self antigens. |
| Cell mediated immunity,T-cell functions? | 1- activation of phagocytes that ingest microbes. 2- killing cells infected with viruses and other parasites. 3- inflammatory response to fungi and helmiths. |
| What is the function of CD4 and CD8? | CD4 and CD8 recognize MHC molecules and activate downstream signals Adhesion molecules facilitate binding of T-cell .CD4 activate phagocytes in tissues and activate B cells in lymphatic follicles, CD8 kill infected cells at the site of infection. |
| What are the molecules involved in T-lymphocyte activation? | CD3 (membrane associated molecules), ITAM ( Immunoreceptor Tyrosine based Activation Motif), ITIM ( Immunoreceptor Tyrosine based Inhibition Motif), B7 -CD29 (co-stimulator MHC with peptide is necessary but not sufficient without B7 expression) |
| What is the region of contact of immune cells called? | Immune synapse where their is a high concentration of ligants and receptors. |
| What is the response to T-cell activation? | 1- CD69 involved in retention of lymphocytes in lymph nodes (down-regulates S1P1 receptor), 2- IL-2 stimulates survival and proliferation, 3- CD40 is an effector molecule, 4- CTLA-4 is an inhibitor of immune response . |
| How is the CD4 T-cell developed and what's the role of CD40L? | Effects are mediated by cytokines including CD40L that binds CD40 on macrophages, dendritic cells and B cells.CD40L and CD40 form positive self-amplification loop for activation of T cells by APCs. |
| What are memory T cells? | They are slowly proliferating supported by IL-7 and IL-15 produced by stromal cells in tissues. |
| What are central memory cells? | They reside in lymphoid organs |
| What are effector memory cells? | They reside in mucosal and other tissues. |
| What is migration controlled by? | Integrins (receptors that bind to the extracellular matrix). , selectins (glycoproteins cell adhesion molecule) ,chemokines (signaling proteins secreted by cells). |
| What is rolling ? | TNF-a and IL-1 induce E-selectin expression on endothelial cells. Thrombin induces translocation of P-selectin to endothelial cell surface.Stable adhesion- chemokines secreted by macrophages and endothelial cells attach to endothelial cells and when bind to neutrophils increase affinity of integrins to integrin ligands on endothelial cells. Endothelial cells are stimulated by TNF-a and IL-1 to express ligands for integrins. |
| Naïve T cells role in cell migration? | Do not express ligands for selectins or chemokines, and therefore do not migrate to infection site. Decline of the immune response. |
| How do Naïve T cells respond to infection? | During the response to the infection the survival and proliferation of effector T-cells is maintained by antigen, co-stimulatory signals from CD28 and cytokines like IL-2. |
| What happened in the absence of stimulation by antigen ? | Lymphocytes die by apoptosis. |
| What happens to effector cells and memory cells after infection? | The number of effector cells subside within 1-2 weeks, when only memory T-cells remain to remember the antigen if another infection happens. |
| What is the first step in neutrophil migration to infection site? | (S1P) regulates exit of T-cells from lymph nodes. Blood has higher levels of S1P comparing to lymph node. |
| What is the second step in neutrophil migration ? | After clonal expansion is over L-selectin and CCRX7 receptor expression is lost and S1P receptor is re-expressed and guides lymphocytes out of lymph node. |
| What is the third step in neutrophil migration | Activated T cells express ligands for E and P-selectins, and integrins LFA-1 and VLA-4. Inflammatory cytokines TNF-a and IL-1 induce expression of E- and P-selectins and ligands for integrins ICAM-1 and VCAM-1. |
| What's the result of cell migration? | As a result effector T-cells roll, adhere and migrate through endothelium at the site of infection/inflammation. |
| What are the major types of hypersensitivity reactions? | 1- Immediate hypersensitivity, ( type I hypersensitivity) 2- Antibody-mediated ( type II hypersensitivity) 3- Immune complex diseases ( type III hypersensitivity) 4- T cell–mediated diseases (type IV hypersensitivity) |
| What's Immediate hypersensitivity, ( type I hypersensitivity)? | A type of pathologic reaction that is caused by the release of mediators from mast cells. This reaction most often depends on the production of immunoglobulin E (IgE) antibody against environmental antigens and the binding of IgE to mast cells in various tissues. (Most frequent of all hypersensitivity,known as allergy or atopy ) |
| What's Antibody-mediated ( type II hypersensitivity)? | Antibodies that are directed against cell or tissue antigens can damage these cells or tissues or can impair their function. (Antibody-mediated (IgM or IgG) against cell surface or extracellular matrix proteins) |
| What's Immune complex diseases ( type III hypersensitivity)? | Antibodies against soluble antigens in the blood may form complexes with the antigens, and the immune complexes may deposit in blood vessels in various tissues, causing inflammation and tissue injury. (Immune complex-mediated (IgM or IgG) against soluble antigens) |
| What's T cell–mediated diseases (type IV hypersensitivity)? | These are diseases that result from the reactions of T lymphocytes specific for self antigens or microbes in tissues. (T cell-mediated, involving pro-inflammatory cytokines and secondary effectors). |
| What are the two types of antigens that cause hypersensitivity? | 1- responses to foreign antigens (microbes and noninfectious environmental antigens) may cause tissue injury, especially if the reactions are repetitive or poorly controlled. 2-the immune responses may be directed against self (autologous) antigens, as a result of the failure of self-tolerance.Responses against self antigens are termed autoimmunity, and disorders caused by such responses are called autoimmune diseases |
| What are the cell types involved in Immediate hypersensitivity ? | B cells, Tfh cell, IgE recreating plasma cells, Mast cells, |
| What are the sequences of events that occur in type 1 Immediate Hypersensitivity? | 1. In response to certain antigens (allergens), a Th2 and Tfh response is activated. Allergens include pollen, food, insect venom, animal dander, penicillin, causing hay fever, food allergies, bronchial asthma and anaphylaxis. 2. Th2 and Tfh secrete IL-4 and IL-13 that induce switching to IgE production by B cells. IgE bind to mast cells via Fc receptor. (Individual becomes sensitized). 3. On second exposure to allergens, Fc-bound IgE binds to antigens and becomes cross-linked. 4a. Crosslinking of surface IgE causes mast cell degranulation with release of vasoactive amines (histamine) causing immediate hypersensitivity: increase in vascular permeability smooth muscle contraction 4b. Other products released from mast cells include cytokines like IL-4 and TNF- that attract eosinophils and neutrophils causing more severe inflammatory response and tissue injury, called the late-phase reaction. |
| What is the late-phase reaction, and how is it caused? | It's when a severe inflammatory response and tissue injury that occurs. A) Kinetics of the immediate and late-phase reactions. The immediate vascular and smooth muscle reaction to allergen develops within minutes after challenge (allergen exposure in a previously sensitized individual), and the late-phase reaction develops 2 to 24 hours later. B) Morphology of the immediate reaction is characterized by vasodilation, congestion, and edema. C) The late-phase reaction is characterized by an inflammatory infiltrate rich in eosinophils, neutrophils, and T cells. This inflammatory component is called the late-phase reaction, and it is mainly responsible for the tissue injury that results from repeated bouts of immediate hypersensitivity. |
| Type II hypersensitivity: what's the Mechanisms of Antibody-Mediated Tissue Injury? | Antibodies against tissue antigens (cells or extracellular matrix) induce inflammation by attracting and activating leukocytes. IgG antibodies bind to neutrophil and macrophage Fc receptors and activate these leukocytes, resulting in inflammation. IgG, as well as IgM antibodies, activate the complement system by the classical pathway, resulting in the production of complement by-products that recruit leukocytes and induce inflammation. When leukocytes are activated at sites of antibody deposition, these cells release reactive oxygen species and lysosomal enzymes that damage the adjacent tissues. |
| Type II hypersensitivity: Mechanisms of Antibody-Mediated Tissue Injury? | If antibodies bind to circulating cells, such as erythrocytes, neutrophils, and platelets, the cells are opsonized and may be ingested and destroyed by host phagocytes. |
| What are some examples of diseases caused by antibodies specific for cell surface or tissue matrix antigens? | Type II hypersensitivity: antibody-mediated diseases: -autoimmune hemolytic anemia (red cell destruction),-autoimmune thrombocytopenia (destruction of platelets), -Graves disease (hyperthyroidism, targeting TSH). |
| How are the clinical manifestations different from most diseases caused by antibodies specific for cell surface or tissue matrix proteins? | Type III hypersensitivity:Diseases Caused By Antigen-Antibody Complexes: -systemic lupus erythematosus, polyarteritis nodosa, serum sickness. Complexes containing positively charged antigens are particularly pathogenic because they bind avidly to negatively charged components of the basement membranes of blood vessels and kidney glomeruli. |
| How do immune complexes cause disease? | Type III hypersensitivity: Immune complexes usually deposit in blood vessels, especially vessels through which plasma is filtered at high pressure (e.g., in renal glomeruli and joint synovium). Therefore, in contrast to diseases caused by tissue antigen-specific antibodies, immune complex diseases tend to be systemic and often manifest as widespread vasculitis involving sites that are particularly susceptible to immune complex deposition, such as kidneys and joints. |
| How do antibodies cause disease without tissue injury? | Some antibodies may cause disease without directly inducing tissue injury. In some cases of myasthenia gravis, antibodies against the acetylcholine receptor inhibit neuromuscular transmission, causing paralysis. Other antibodies may directly activate receptors, mimicking their physiologic ligands. For example, Graves disease, in which antibodies against the receptor for thyroid-stimulating hormone activate thyroid cells even in the absence of the hormone. |
| Diseases Caused by T Lymphocytes? | 1-cytokine-mediated inflammation. 2-T-cell-mediated killing of host cell. |
| What happens in cytokine-mediated inflammation? | Inflammation may be triggered by cytokines produced mainly by CD4+ T cells in which tissue injury is caused by activated macrophages and inflammatory cells. Excessive polyclonal T cell activation by certain microbial toxins produced by some bacteria and viruses can lead to production of large amounts of inflammatory cytokines, causing a syndrome similar to septic shock. These toxins are called superantigens because they stimulate large numbers of T cells. |
| What happens in T-cell-mediated killing of host cell? | Direct killing of target cells is mediated by CD8+ cytotoxic T lymphocytes (CTLs) |
| What are some examples of diseases caused by T cells? | T cell–mediated autoimmune diseases are usually limited to a few organs and usually are not systemic. Examples of T cell–mediated hypersensitivity reactions against environmental antigens include contact sensitivity to chemicals like therapeutic drugs and substances found in plants ( poison ivy)). Tissue injury also may accompany T cell responses to microbes. For example, in tuberculosis, a T cell–mediated immune response develops against protein antigens of Mycobacterium tuberculosis, and the response becomes chronic because the infection is difficult to eradicate. The resultant granulomatous inflammation causes injury to normal tissues at the site of infection. |
| The role of superantigens in type IV hypersensitivity? | They are Toxins that stimulate large numbers of T cells. Superantigens bind to invariant parts of T cell receptors on many different clones of T cells, regardless of antigen specificity, thereby activating these cells. |