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T Leandersson

Publications and source records attributed to T Leandersson.

6 recordsLinked to original sources
PubMed2006

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. The IgM response to a T-cell-dependent antigen was reduced in JDTA mice but still easily detectable. In contrast, a very pronounced primary IgA response could be detected in JDTA mice while wild type controls showed no detectable primary IgA response. With regard to naturally occurring antibodies, bone marrow chimeras between JDTA and control C57BL/6 mice had a donor cell phenotype with regard to serum IgM and IgA. Mixed bone marrow chimeras had an intermediate phenotype, indicating that the naturally occurring antibody IgM and IgA levels are B-cell autonomous and not subjected to feed-back control. This was confirmed by transfer of the dominant naturally occurring IgM/IgA phenotype to the recipient by peritoneal exudate cells.

Animals↗
PubMed1993

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. Spleen cells obtained at 21 dpi showed a lower Con A proliferative response and IL-2R expression compared with non-infected controls, while the proliferation and IL-2R expression of lymph node cells at 21 dpi was unaltered. Supernatants from 48 h Con A-stimulated spleen and lymph node cells from mice at 21 dpi had very low levels of IL-2 but contained significantly higher levels of IFN-gamma compared with the supernatants of cells from non-infected mice. The latter phenomenon correlates with an accelerated rate of IFN-gamma mRNA accumulation.

Animals↗
PubMed1984

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. These results are ascribed to the activity derived from normal T cells, with the same characteristics as BSF-p1 previously obtained from lymphomas and hybridomas. Since hybridization of these T helper cells results in the constitutive production of BSF-p1 in the absence of macrophages, these experiments demonstrate that BSF-p1 is a normal T-cell product.

Animals↗
PubMed1984

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. Classical in vivo observations and our in vitro experiments led us to conclude that induction of B cells does not occur upon binding of T cell-dependent antigens to Ig receptors and, consequently, that B lymphocyte activation by anti-receptor antibodies has no physiological counterpart. Induced B lymphocytes proliferate and mature to high rate secretion of antibodies under the influence of selective growth and maturation factors produced by helper cells which are MHC-unrelated, act polyclonally and have no influence in normal, resting cells. Specific ligand interactions with the membrane molecules participating of that functional complex may also regulate reactivity to either growth or maturation factors, and, thus, control clonal performances and the fate of activated cells.

Animals↗