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Adaptive Immunity


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Positive selection
is the apoptosis of immature T/Bcells when their receptors bind to weakly to MHC and are thus unable to recognise MHC-antigen complexes
Negative selection
is the apoptosis of immature T/Bcells when their receptors bind to strongly to MHC and are thus reactive to self antigens
MHC I
is displayed on all nucleated cells, when angiten-MHC forms this marks the cell as infected to CD8+ T cells/NK cells
MHC II
is used by APCs to present antigen epitopes to T cells.
Antigen presenting cells
include dendritic cells, macrophages and B lymphocytes (Bcells) with MHC class II
Somatic recombination
of V, D and J segments of the variable region of Ig genome causes hypermutation and thus the variation in antigen binding site (light chains) of different Bcells
CD40
ligand is secreted by activated Tcells to the corresponding antigen presenting Bcell in order to activate that Bcell
Peripheral lymphoid tissue
provides an environment where naïve Bcells can interact with CD4 Tcells sensitive to the antigen being presented.
Plasmablasts
are partially activated Bcells that are still able to divide, hypermutate, class switch and express MHC while secreting Igs
IgG
main Ig that caused opsonisation, agglutination, complement activation and toxin neutralisation. Only Ig to cross placenta.
IgM
forms Ig polymers, increasing avidity and thus allowing antigen binding without prior immunization (=natural Ig). Often first Ig in response to infection. Activates complements (3b = opsonisation)
IgA
most common Ig in mucosal areas. Poor complement activator and opsonises weakly. Instead activates degranulation and cytotoxic cells.
IgE
primes allergen response by binding to FcεR receptors on mast cells and basophils causing degranulation
IgD
along with IgM is a surface Ig on Bcells. Involved in antigen recognition and possibly activation of basophils and mast cells.
Double positive Tcells
express both CD4 and CD8 TCRs and differentiate depending on whether their TCR recognises MHCI of infected cells (=CD8) or MHCII of APCs (=CD4) with higher affinity.
B7 proteins
are secreted by APCs and bind to CD28 receptors on Tcells to, along with antigen presentation/recognition, activates CD4/8 Tcells
T helper 1 cells
mediate destruction of intracellular bacteria by secreting cytokines (IFNγ, TNFβ, IL-10) to activate macrophages and CD8 Tcells
T helper 2 cells
mediate allergic responses and control parasites by recruiting eosinophils, mast cells and basophils from bone marrow and promote Bcell class switching to IgE
T helper 17 cells
recruit neutrophils in early response to infection by inducing epithelial/fibroblast cells to secrete chemotactic cytokines
T follicular helper cells
activate Bcell production of strongly opsonising Igs by secreting IFNγ and induce class switching to IgE by IL-4
T regulatory cells
suppress Tcell activity thus preventing overzealous immune response by secreting cytokines that inhibit Tcell proliferation and DC differentiation
Interleukin II
is a potent autocrine Tcell growth factor that causes clonal expansion of activated Tcells