MT A 1 Flashcards
Property of the human immune system to avoid attacking its own cells.
Tolerance
Organs in which self-tolerance is acquired through recognition of self antigens.
Thymus and bone marrow
In central tolerance, after antigen presentation, immature T cells become
T regulatory cells
Mechanism of the body to develop central tolerance to Ag not present in blood stream but in tissues.
AIRE protein creates tissue-restricted antigens (TRAs) from tissular DNA.
Process through which T cells that do not recognize self Ag disappear
Negative regulation
T cell receptor that after being bound by an ACP B7 costimulator elicits an immune response.
CD28
Peripheral tolerance works though the expression of this inhibitory receptor that binds to CD28 on the T cells thus suppressing response.
CTLA-4
T reg cells express CTLA-4 that binds to B7 in ACP to
Remove B7 from the ACP
Regulatory T cells express this gene to inhibit responses to self antigens.
FOXP3
Cytokine that promotes differentiation of T cells from immature to T regs
IL-2
Immunosuppressive cytokines produced by T regs
IL-10 and TGF-B
Protein in intrinsic apoptosis that binds to Bcl-2 factors (Bax and Bak) to create pores in mitochondrial membrane.
BH3
Cytochrome c activates this enzyme in intrinsic apoptosis to fragment DNA
Endonuclease
Ligand in T cells necessary for endonuclease activation in extrinsic pathway apoptosis.
FasL
Substance necessary for extrinsic pathway apoptosis
TNF
Mechanism of action of central tolerance on B cells.
Light chain of antibody to self antigens is modified so it cannot bind
Gene most strongly associated to ankylosing spondylitis
HLA B27
Type of tolerance used for Ag not present in generative lymphoid organs and Ag expressed only in adult life.
Peripheral tolerance
Cells in charge if mantaining peripheral tolerance by supressing activation of lymphs for self Ag.
T regs
Death of immature cells that recognize antigens in the thymus
Deletion or negative selection
Protein of the thymus that allows medullary thymic epithelial cells (MTECS) to produce Ags of peripheral tissues.
AIRE protein
Disease of AIRE protein failure.
Autoimmune polyendocrine syndrome type 1 (APS1)
Cells become unresponsive to self antigens through lack of costimulation or innate immunity, or through engagement of inhibitory receptors
Anergy
Peripheral tolerance mechanism in which T cells activation will be blocked by a T reg cells
Supression
Mediator that a self-reacting T cell will express in peripheral tolerance to terminate response intrinsically
CTLA-4
Function of CTLA-4 in self reacting T cells to supress response
Remove B7 from APC leading to a lack of costimulation
Cytokin on which T regs depend for differentiation, survival and function.
IL-2
Immunosupresive cytokines produced by T regs
IL-10 and TFG-B
Proteins of the apoptosis intrinsic pathway in peripheral tolerance deletion
Bcl-2 family effectors (Bax and Bak)
Apoptosis extrinsic pathway interactions
Fas-FasL
TNF R - TNF
Rutas de administración que favorecen la tolerancia
Intravenosa y mucosa
Central tolerance mechanisms for high-avidity self reacting B-cells
Receptor editing through expression of new Ig light chain (non self reacting)
Apoptosis (deletion)
Central tolerance mechanism for low avidity self reacting B-cells
Reduced expression of receptor and signaling (anergy)
Peripheral tolerance mechanism to self-reacting B-cells
Anergy
Deletion
Regulation by inhibitory receptors
A self reaction to one specific antigen leads to alterations of other tissue antigens.
Epitope spreading
Cells activated in an infection that may lead to autoimmunity and that overly-active T cells.
APCs
Genes that have shown stronger association with autoommunity.
MHC genes
Stronges genetical-autoimmunity relation.
Ankylosing spondylitis and HLA B27
Gene associated with SLE
C4
Gene associated with T-cell proliferation and infiltration in organs, leading to systemic inflammatory disease
CTLA4
Disease related to Fas/FasL, in which self-reactive B cells and CD4 T are not deleted
ALPS
Tregs won’t work due to a FoxP3 alteration, creating multiorgan lymphocytic infiltrates, leading to
IPEX
Inflammatory bowel disease, in which there is a deffective control in mucosal immune responses, relates to the genes of…
IL10 and IL10R
Leucocitos reclutados en reacciones de hipersensibilidad tipo II: mediada por anticuerpos
Neutrófilos y macrófagos
Reacción de hipersensibilidad mediada por inmunocomplejos con IgM o IgG
Tipo III
La participación de CD4 Th1 y Th17 y CD8 CTLs es característica de la hipersensitividad
IV
Mecanismos de daño tisular en la reacción de hipersensibilidad tipo IV
Inflamación mediada por citocinas y activación de macrófagos y muerte celular directa
IL de la hipersensibilidad mediada por IgE
IL4, IL5 e IL13
En la anemia hemolítica y trombocitopenia autoinmune, hay una destrucción tras opsonización.
Hipersensibilidad de tipo:
II
En Graves disease hay una alteración de las funciones celulares sin inflamación ni daño tisular. Hipersensibilidad de tipo:
II
Un ejemplo de esta hipersensibilidad es la unión de anticuerpo a un receptor de hormonas/neurotransmisores y su estimulación.
Tipo II
Most predominant lekocytes in type III hypersensitivity inflammation.
Neutrophil
Function of IL17 secreted by TH17 cells
Neutrophil recruitment
Function of IFNy secreted by TH1 cells
Macrophage activation
Reaction that develops 24 to 48 hrs after Ag challenge in a previously immunized individual
Delayed-type hypersensitivity DTH
If a Th1 response to an infection activates macrophages but fails to eliminate microorganisms it happens a___
Chronic DTH reactions causing granulomas
Explicación del diagrama
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Tipo de hipersensibilidad que causa glomerulonefritis
Tipo II