Analysis of antigen-specific and naturally occurring IgM and IgA steady-state levels in J-chain negative C57BL/6 mice.

Naturally occurring IgM and IgA levels are remarkably stable between different individuals. In mice lacking joining chain (J-chain), the steady-state levels of IgM are reduced, while IgA levels are elevated. We have here analysed the IgM and IgA responses as well as the regulation of naturally occurring antibodies in mice that delete all J-chain expressing B cells (JDTA mice) and have been back-crossed to C57BL/6 mice.

Organ-specific regulation of interferon-gamma, interleukin-2 and interleukin-2 receptor during murine infection with Trypanosoma cruzi.

We have studied the expression of IFN-gamma, IL-2 and IL-2 receptor (IL-2R) at the mRNA and protein levels in spleen and lymph node cells from Trypanosoma cruzi-infected BALB/c mice. At 21 days post infection (dpi) (peak of parasitaemia), spleen cells stimulated with Con A for 16 h showed a reduced IFN-gamma, IL-2 and IL-2R mRNA production compared with non-infected controls. Lymph node cells obtained at 4, 21 or 60 dpi produced similar amounts of IFN-gamma, IL-2 or IL-2R transcripts after mitogen stimulation as uninfected controls.

Functional and chemical characterization of B-cell growth factor produced by normal cloned T helper cells.

Media conditioned by clones of normal helper T cells exposed to appropriate antigen-presenting cells contain growth-promoting activity for B-cell blasts induced either by lipopolysaccharide or on direct interaction with competent helper cells. This B-cell growth factor (TH-BGAPet) is recovered on sodium doecyl sulphate polyacrylamide gel electrophoresis corresponding to mol. wt of 15,000-20,000 displays no mitogenicity for small, non-induced B lymphocytes and is completely devoid of the ability to activate immunoglobulin secretion in proliferating B cells.

T cell-dependent B cell activation.

T cell-dependent induction of small, resting B lymphocytes requires direct recognition of antigen and/or I-A/E molecules on the B cell surface by the inducing helper cell, and it does not require the participation of Ig receptors on the responding B cell. Triggering B cell receptors, therefore, are either the I-A/E molecules themselves, or other structures with complementarities on helper cell membranes that become available for productive interactions upon I-A/E recognition. It would appear that signal delivery by such triggering receptors can be regulated by a membrane complex of molecules, involving immunoglobulins, Class II MHC molecules and other classes of receptors, which in selective and distinct manners control the quantitative levels of expression and/or availability of the relevant structures.