5-6-dichloro-1-beta-d-ribofuranosylbenzimidazole-3--5--monophosphorothioate and pelargonic-acid

Retention of T cells within affected tissue is a critical component of adaptive immune inflammation. However, the mechanisms involved in T cell retention remain largely undefined. Previous studies revealed the capacity of cAMP signaling to regulate immune cell migration, as well as dynamic regulation of receptors that could induce cAMP production in immune cells. The potential for cAMP to act as a retention signal has been mostly unexplored, partially as a result of this second messenger's well-characterized inhibition of effector function in immune cells. Here, we report that cAMP regulates the tissue retention of mouse T cells at concentrations well below those that inhibited proliferation or decreased acquisition of an effector phenotype. Stimulation of CD4

Topics: Adaptive Immunity; Animals; Animals, Congenic; Antigens, CD; Antigens, Differentiation, T-Lymphocyte; CD4-Positive T-Lymphocytes; Cell Line, Tumor; Cells, Cultured; Chemokine CCL21; Chemokine CXCL12; Chemotaxis, Leukocyte; Colforsin; Cyclic AMP; Dicarboxylic Acids; Dichlororibofuranosylbenzimidazole; Fatty Acids; Hydrazones; Isoxazoles; Lectins, C-Type; Lymphocyte Activation; Mice; Mice, Inbred C57BL; Odorants; Receptors, Odorant; Thionucleotides