Very low affinity B cells form germinal centers, become memory B cells, and participate in secondary immune responses when higher affinity competition is reduced.

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To understand the relationship between the affinity of the B cell antigen receptor (BCR) and the immune response to antigen, two lines of immunoglobulin H chain transgenic (Tg) mice were created. H50Gmu(a) and T1(V23)mu(a) mice express mu H chain transgenes that associate with the lambda1 L chains to bind the (4-hydroxy-3-nitrophenyl)acetyl hapten with association constants (K(a)s) of only 1.2 x 10(5) M(-1) and 3 x 10(4) M(-1), respectively. Both lines mounted substantial antibody-forming cell (AFC) and germinal center (GC) responses. H50Gmu(a) Tg mice also generated memory B cells. T1(V23)mu(a) B cells formed AFC and GCs, but were largely replaced in late GCs by antigen-specific cells that express endogenous BCRs. Thus, B lymphocytes carrying BCRs with affinities previously thought to be irrelevant in specific immune responses are in fact capable of complete T cell-dependent immune responses when relieved of substantial competition from other B cells. The failure to observe such B cells normally in late primary responses and in memory B cell populations is the result of competition, rather than an intrinsic inability of low affinity B cells.







Garnett H. Kelsoe

James B. Duke Distinguished Professor of Immunology
  1. Lymphocyte development and antigen-driven diversification of immunoglobulin and T cell antigen receptor genes.
    2. The germinal center reaction and mechanisms for clonal selection and self - tolerance. The origins of autoimmunity.
    3. Interaction of innate- and adaptive immunity and the role of inflammation in lymphoid organogenesis.
    4. The role of secondary V(D)J gene rearrangment in lymphocyte development and malignancies.
    5. Mathematical modeling of immune responses, DNA motifs, collaborations in bioinformatics.
    6. Humoral immunity to influenza and HIV-1.

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