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T helper cell‐dependent B cell activation
Author(s) -
Noelle Randolph J.,
Snow E. Charles
Publication year - 1991
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.5.13.1833257
Subject(s) - antigen , microbiology and biotechnology , major histocompatibility complex , b cell , b cell receptor , biology , antigen presenting cell , naive b cell , antibody , antigen presentation , mhc restriction , mhc class ii , immunology , mhc class i , chemistry , t cell , immune system
Small, resting B lymphocytes are driven into the cell cycle as a consequence of receiving multiple signals from elements found within their local environment. The first of these signals results from the binding of specific antigen to membrane immunoglobulin (mIg) receptors on the B cells. Pursuant to antigen binding, signals are transduced and the B cell commences to endocytose and degrade the antigen. Fragments of the antigen are expressed on the B cell surface in noncovalent association with class II major histocompatibility complex (MHC) molecules. The antigen‐class II MHC complex serves as a recognition complex for CD4 + helper T cells (T h ). As a consequence of recognition, T h form stable physical conjugates with the B cells. Over an extended period of time the T h and B cells bilaterally signal one another. This interchange of signals results in the growth and differentiation of both cells. This review will discuss the sequence of events that culminate in the growth and differentiation of B lymphocytes to antibody‐producing cells.—Noelle, R. J.; Snow, E. C. T helper cell‐dependent B cell activation. FASEB J. 5: 2770‐2776; 1991.