ADAPTIVE IMMUNITY

Adaptive immunity Specific Slow during the primary response, but very fast during the secondary responses memory

Specificity is achieved by BCRs and TCRs Each B cell express a unique BCR and each T cell express a unique TCR Clonal selection!

B cell receptor (BCR)

HUMORAL RESPONSE Circulating B cells which have not been exposed to the antigen  naive B cells When BCR binds to the antigen, the antigen is internalised by the B cell and presented to the T cells

Activated t cells induce -Cell surface proteins (CD40L) -Cytokines -Activated B cell divide rapidly and differntiate to plasma cell -This events take in germinal centres of lymphnodes and spleen

The first IG is always IgM Later different cytokines instruct B cells to secrete different IG classes (isotype switching)

IG diversity Differnt gene segments on different chromosomes encode heavy and light chains These multigene families are separated by non-coding regions and are brought together with gene rearrengements.

Light chain V  about 76 J  5 C  1 Heavy chains V  D  27 J  9 C  11 Recombinase activating gene RAG-1 and RAG 2  recombinase responsible for the VDJ recombination

Isotype switching: IL-4  IgG and IgE IL-5  IgA DNA sequences known as “switch sites” are located upstream of heavy constant region on the DNA (M, D, G, E and A) IgM and IgD do not have switch sites Affinity maturatin  Somatic hypermutation (random mutationx in V regions)

Cell mediated immunity CMI is the major component of immune response T cell are essential cells influencing Cytokine production, B cell activation, macrophage activation, rejection, killling of tumor or infected cells, DTH

TCR Gamma-delta TCR bearing cells are found in skin, epitelial and intestinal layers Antigen recognition is MHC restricted Alfa-gamma  V, D and J; Beta, delta  V and J rearrengements No somotic hypermutation

TH17 CD4+ cells producing IL-17 and 22 Early immune response to bacteria Autoimmunity Immunity against fungi

Treg CD4+CD25 + FOXP3