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Immunology Final
Autoimmunity, Lec 24
| Term | Definition |
|---|---|
| What causes Autoimmune diseases? | inappropriate immune responses against self tissues/organs that lead to tissue or organ damage |
| _____ are immune responses against self antigens (autoantigens) which are tolerated in normal conditions | Autoimmune responses |
| Both ____ and ____ responses result in _________ and various degrees of tissue damage. | B cells, T cells, chronic inflammation |
| Why can't the immune system completely distinguish between self and non-self antigens? | The difference between Pathogen Ag and self Ag are very subtle at the molecular level. |
| What are 3 mechanisms of self tolerance? | 1) Central tolerance 2) Peripheral tolerance 3) Sequestration of self-antigen |
| What is the goal of self-tolerance in the immune system? | ELIMINATE self reactive lymphocytes and INHIBIT ACTIVATION of self reactive lymphocytes. |
| _____ induce immune TOLERANCE and usu. have sustained presence in high concentrations. ____ induce immune RESPONSE and usu. appear suddenly with increased concentration over time. | Auto-antigens, Pathogen antigen |
| Where is Central Tolerance? | Tolerance that is induced during lymphocyte development (negative selection) |
| In central tolerance, if there is High affinity for Self Ag then ________, if there is Intermediate affinity for Self Ag then ______, and if there is Low affinity for Self Ag then _____. | Receptor editing or cell death occurs, nTreg cells are produced, Mature naive T cells are produced |
| What IS self-tolerance? | When the immune system responds against self Ags (autoAgs) which are tolerated in normal conditions |
| Where is Peripheral Tolerance? | Tolerance induced in mature lymphocytes |
| In peripheral tolerance, recognition of self-Ag w/out costimulatory interaction leads to _____. Also, _____ are produced. | Activation of mediated cell death or anergy, iTreg cells (inducible Treg) |
| Where is Sequestration of Self-Ag? | sites that are not nonrmally accessible to lymphocytes: eye, brain, testis |
| What cells mediate self-tolerance? | Treg cells! |
| What are two populations of regulatory T cells? | nTregs and iTregs |
| _____ develop in the thymus and react to self-Ag. It passes + selection but not strong enough to induce Apoptosis. ____ are activated as naive T cells and diff. under ____ without ___ | nTreg T cells, iTreg T cells, TGF-beta IL-6 |
| What are the functions of Treg cells in self-tolerance? | 1) Treg CTLA-4 bind to CD80/86 on APC reducing express of costim mol and proinflam cytokines 2) Produce immune SUPPRESSIVE CYTOKINES(IL-10,TGF-beta) to inhibit effector T cells 3) LINKED SUPPRESSION = suppress effector T cels binding to same APC |
| A defect in the ____ gene causes _____ (APD) or polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) | AIRE gene, autoimmune polyglandula disease |
| A defect in the ____ which is a defect in _____ causes _____, _____, ______, and _____ (IPEX). | FoxP3 gene, Treg development, Dysregulation, Polyendocrinopathy, Enteropathy, X-linked syndrome |
| Why is it suggested that autoimmune responses are related to presentation of specific Auto Ags to T cells? | Bc most autoimmune diseases are related to certain HLA allotypes/haplotypes esp. with HLA Class 2. |
| What are the environmental factors that influence the onset of autoimmune disease? | Smoking and infection |
| Sequestration of Self-Ags such as eyes that are exposed to the immune system after trauma can cause ______, which means _____. | Sympathetic ophthalmia, Auto-effector cells induced from an injured eye can cause damage to the non-injured eye. |
| What are 3 sources of self-antigens in autoimmunity? | exposure to normally non-accessible Ag, altered self proteins, and molecular mimcry |
| ______ is an autoimmune disease where _____ (PAD) converts ___________. This altered peptide is presented to CD4 T cells by _____ to induce Ab response to them. | Rheumatoid arthritis, peptidyl arginine deiminase, arginine to Citrulline, HLA DRB1*04 |
| What is molecular mimicry? | pathogen components have antigenic similarity with self Ag and immune responses react to both causing tissue damage and autoimmune response |
| Rheumatic fever, an autoimmune response, is caused by _____ where some Abs cross-react to epitopes on ________ which can activate complement and stimulate inflammation. | Streptococcus pyogenes, heart kidney and joint tissues |
| Many autoimmune diseases are initiated by infection or tissue trauma bc _____ interaction and ______ play important roles in activation/differentiation of auto T cell response | PAMP-PRR interaction, DC activation |
| For ________ effects of infection, ignorant or anergized auto-reactive T cells may be activated during infection, bc expressed cytokines (____) favor _______ reduction and _____. | Antigen non-specific, TGF-beta+IL-6, Treg differentiation reduction, Th-17 differentiation |
| For ______ effects of infection, pathogen specific effector T cells may have _________ which cause them to react to self Ag and cause autoimmunity. | Antigen specific, cross-reactivity to self Ag |
| Infection can also stimulate ________ on cells that don't normally express this and _______. This can cause exposure of ____ to be presented to CD4 T cells that are not well tolerated. Example, _____. | MHC Class 2 expression, enhance presentation of Self Ag, Cryptic Ag, Cryptic thyroid Ag |
| What is Systemic Lupus Erythemotosus (SLE)? | intermolecular EPITOPE SPREADING where auto-Abs progressively increase reactivity to more self-Ags |
| _________ is when B cells to DNA can endocytose whole nucleosome and present H1 peptides on MHC class 2 to get H1 specific T cell help | T,B cell linked Ag recognition |
| H1 specific B cells serve as _______ and can endocytose whole nucleosomes and present various peptides to CD4 T cells specific to Different nuc pep to activate THEM, which in turn can help other Auto-B cells | Ag presenting cells |
| _____ is an intramolecular epitope spreading autoimmune response where Auto-Ab to Desmolein expands to different epitopes, called ______. Auto-Ab can expend initially from one epitope ____ to multiple epitopes on the same molecule ___. | Pemphigus foliacegus, desmolein-intramolecular epitope spreading, EC5 no clinical disease, EC1 disease |
| Autoimmune disease have similar pathogenic mechanisms as ______. | Hypersensitivity |
| Autoimmune diseases can be ______ (like type 1 diabetes) or more _______ (systemic lupus erythematosus). Most autoimmune diseases are _____ since Anti-Ags are always present. | Organ specific, systemic, chronic |
| Many autoimmune diseases are mediated by ______ (auto-Ab or auto-reactive T cells) and can be classified into three types _____, corresponding to its hypersensitivity type. | a dominant auto-immune response, Type 2 3 4 |
| There is no _______ (it's an antibody) mediated autoimmune disease. | IgE |
| Type __ autoimmunity is mediated by Ab to cell surface or extracellular matrix, and examples are ____, _____, and ______. | 2, Goodpastures syndrome, Grave's disease, Hashimoto's disease |
| In Goodpature's syndrome, ______ IgG binds to basement membrane of many tissues esp in glomeruli of kidney that activates ___ via Fc receptor. Activated cells secrete inflammatory cytokines/chemokines recruit more leukocytes and cause tissue damage | Type 4 collagen, Macrophages neutrophils and mast cells |
| In Graves disease, __________ acts as an agonist to activate thyroid hormone secretion. It is also called a _____. | autoantibody to thyroid stimulation hormone (TSH) receptor, Hyperthyroid condition |
| In Hashimoto's disease, Th1 and Ab responses to thyroid cause inflammation by lymphocyte infiltration also called ______. Auto Ab is also generated against thyroid . Inflammation that causes thyroid damage is called a _____ | ectopic lymphoid tissues, hypothyroid condition |
| What happens in Systemic Lupus Erythematosus (SLE)? | patients have a defect in removing apoptotic cells; dead cells release intracellular Ags and stimulate auto-Ab responses (anti-DNA or nucleoprotein Ab) |
| Type ___ autoimmunity is mediated by Ab-Ag complexes | 3 |
| _____ deposit on small blood vessels of many organs and tissues, activate leukocytes via ___ and induce a destructive chronic inflammatory response, just like Type __ hypersensitivity. Ab to ____ is important for diagnosis | Auto-Ab-Ag immune complexes, Fc receptors, 3, dsDNA |
| Type ___ autoimmune response is a T cell mediated response | 4 |
| In Type 1 diabetes (insulin dependent diabetes mellitus), T cells (_____) and Ab to pancreas beta-cell components (insulin) induce inflammation and beta cell destruction, called _____. | CD8+CTL, insulitis |
| In Rheumatoid arthritis, ____ is the infiltration of lymphocytes (CD4, CD8 T cells, B cells, plasma cells) and inflammatory cells (neutrophils and MOs), the production of inflammatory cytokines (TNF-a, IL-1, IL-6) and chemokines resulting chronic inflam | Joint synovium |
| What is Rheumatoid factor? | Anti-Ig Ab and IgG form immune complexes, mostly IgM Abs the act against the Fc portion of self IgG. |
| Multiple sclerosis (MS) is a Type __ autoimmune response where auto-reactive T cells and Ab act against _____ in the myelin sheath of nerve fiber in the central nervous system CNS | 4, Myelin Basic Protein MBP, |
| What is demyelination? | damage to myelin sheath caused by anti-MBP antibody after amplified inflammation due to activated Th1, IFN-gamma, Th17, and IL-17 |
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Hamncheese52
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