@article {542171,
	title = {CD80 expression on B cells regulates murine T follicular helper development, germinal center B cell survival, and plasma cell generation.},
	journal = {J Immunol},
	volume = {188},
	number = {9},
	year = {2012},
	month = {2012 May 1},
	pages = {4217-25},
	abstract = {Germinal center (GC) B cells and T follicular helper (T(FH)) cells interact in the production of high-affinity long-lived plasma cells (PCs) and memory B cells, although the mechanisms regulating the formation of these long-lived populations remain unclear. Because CD80 is one of the few markers shared by human and murine memory B cells, we investigated its role in the development of GCs, memory cells, and PCs. In CD80-deficient mice, fewer long-lived PCs were generated upon immunization compared with that in B6 controls. In concert, the absence of CD80 resulted in an increase in apoptotic GC B cells during the contraction phase of the GC. CD80(-/-) mice had fewer T(FH) cells compared with that of B6, and residual T(FH) cells failed to mature, with decreased ICOS and PD-1 expression and decreased synthesis of IL-21 mRNA. Mixed bone marrow chimeras demonstrated a B cell-intrinsic requirement for CD80 expression for normal T(FH) cell and PC development. Therefore, B cell expression of CD80 plays a critical role in regulating B-T interactions in both early and late GC responses. This, in turn, results in impaired ability to produce long-lived PCs. These data provide new insights into the development of GCs and Ab-forming cells and the functions of CD80 in humoral immunity.},
	keywords = {Animals, Antigens, CD80, Antigens, Differentiation, Apoptosis, Cell Survival, Cells, Cultured, Germinal Center, Humans, Immunity, Humoral, Inducible T-Cell Co-Stimulator Protein, Interleukins, Mice, Mice, Inbred BALB C, Mice, Knockout, Plasma Cells, Programmed Cell Death 1 Receptor, RNA, Messenger, T-Lymphocytes, Helper-Inducer},
	issn = {1550-6606},
	doi = {10.4049/jimmunol.1102885},
	author = {Good-Jacobson, Kim L and Song, Eunice and Anderson, Shannon and Sharpe, Arlene H and Shlomchik, Mark J}
}
