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  • 1
    Electronic Resource
    Electronic Resource
    On the Molecular Basis of T Helper Cell Function (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 19 (1984), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: B-lymphocyte promotor factors (B-LPF) are defined as T-cell-derived, released molecules that trigger polyclonal induction of B-cell differentiation into antibody-forming cells. B-LPF activity is independent of antigen, and it apparently induces only IgM-producing B cells. B-LPF was discovered as products of an antigen-specific. I-Ab-restricted T-cell line. We here show that B-LPF is produced also by lymphoma cells derived from this T-cell line or by T-cell hybrids constructed by fusing the T-cell line with BW5147 thymoma cells. A chicken gamma globulin-specific T-cell hybridoma clone also produced B-LPF. Biological assays demonstrated that B-LPF-containing supernatants did not contain IL-1, IL-2, B-cell growth factor, or allogeneic effector factor. Biochemical studies showed that B-LPF was precipitated by 50% (NH4)2SO4 saturation iind that at least three types of molecules were involved in B-LPF activity: molecules with molecular weights of 〉90,000, 50,000–90,000 and 10,000–25,000.The relationship between B-LPF and antigen-specific helper/inducer factors is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1984.tb00967.x
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  • 2
    Electronic Resource
    Electronic Resource
    On the Molecular Basis of T Helper Cell Function (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 19 (1984), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The differentiation of Ig+ B cells into plaque-forming cells is dependent on antigen and factors produced by T cells and/or macrophages. We describe here the production of T-cell factors termed lymphocyte promotor factors (LPF). A foetal calf serum-specific T-cell line and its clones synthesize LPF, which is defined as factors that polyclonally stimulate normal spenic T cells to differentiate into cytotoxic T lymphocytes (T-LPF) and normal splenic B cells to differentiate into plaque-forming cells into (PFC) (B-LPF) in the apparent absence of specific antigen. The proliferation of and the B-LPF production of all T-cell clones tested were foetal calf serum-specific and I-Ab-restricted. Some of these clones produced only T-LPF, some clones produced only B-LPF, and some clones produced both T-LPF and B-LPF. B-LPF stimulate the polyclonal differentiation of Ig+ B cells into PFC without the apparent need for helper T cells, is different from T-LPF, and induces almost exclusively IgM PFC. The B-LPF described in the present paper are compared with previously described T-cell factors, which stimulate antigen-specific B-cell responses or bystander B-cell responses. The conclusion is that B-LPF are probably different from B-cell growth factors, T-cell replacing factors, allogeneic effector factors, and interleukin 2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1984.tb00966.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Role of neutrophils in murine cryoglobulinemia (1998)
    Springer
    Inflammation research 47 (1998), S. 145-150 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Vasculitis — Glomerulonephritis — Cryoglobulins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Murine IgG3 anti-IgG2a rheumatoid factor (RF) monoclonal antibodies (mAb) with cryoglobulin activity, are able to induce, in normal mice, skin leukocytoclastic vasculitis and lupus-like glomerulonephritis resembling ‘wire-loop’ lesions (subendothelial immune deposits). The development of glomerular, but not skin, lesions in immunoglobulin-deficient mice (lacking the corresponding IgG2a autoantigen) receiving IgG3 RF cryoglobulins indicates that the RF activity of IgG3 monoclonal cryoglobulins and subsequent formation of IgG3-IgG2a immune complexes play a critical role in the development of skin vasculitis. In contrast, nephritogenic activity is solely contributed by IgG3-associated cryoglobulin activity. Polymorphonuclear leukocyte (PMN) infiltration is one of the major pathologic changes observed in both types of lesions. Treatment with mAbs against the adhesion molecules leukocyte function-associated antigen 1 (LFA-1) and intercellular adhesion molecule 1 (ICAM-1) (both known for their involvement in PMN-endothelial cell interaction) inhibits the development of skin vascular lesions. However, it has no effect on the generation of glomerulonephritis. Apparently, adhesion molecule requirements for PMN interaction with glomerular capillary endothelial cells are different from those for PMN infiltration of the skin. However, the PMN depletion experiment has clearly shown that PMNs play an active role in the development of ‘wire-loop’ glomerular lesions. In the absence of the glomerular PMN infiltration, IgG3 RF cryoglobulins induce a different type of glomerular lesion, characterized by voluminous intracapillary thrombi and mesangial deposits, yet lacking subendothelial deposits. This is consistent with the fact that the latter lesions can be induced by certain IgG3 mAbs, which are unable to provoke glomerular PMN infiltration. Finally, the activation of the complement system does not appear to play a major role in either skin or glomerular lesions induced by IgG3 RF cryoglobulins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050305
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    Paper (German National Licenses)
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