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Results: 11 to 12 of 12

Publication Record


Modulation of allergic inflammation in mice deficient in TNF receptors.
Rudmann DG, Moore MW, Tepper JS, Aldrich MC, Pfeiffer JW, Hogenesch H, Tumas DB
(2000) Am J Physiol Lung Cell Mol Physiol 279: L1047-57
MeSH Terms: Aerosols, Animals, Asthma, Bronchoalveolar Lavage Fluid, Disease Models, Animal, Immunoglobulin E, Immunoglobulin G, Interferon-gamma, Interleukin-2, Interleukin-4, Interleukin-5, Mice, Mice, Inbred C57BL, Mice, Knockout, Ovalbumin, Pneumonia, Receptors, Tumor Necrosis Factor, Respiratory Hypersensitivity, Signal Transduction, T-Lymphocyte Subsets, Tumor Necrosis Factor-alpha
Show Abstract · Added February 26, 2014
Tumor necrosis factor-alpha (TNF) is implicated as an important proinflammatory cytokine in asthma. We evaluated mice deficient in TNF receptor 1 (TNFR1) and TNFR2 [TNFR(-/-) mice] in a murine model of allergic inflammation and found that TNFR(-/-) mice had comparable or accentuated responses compared with wild-type [TNFR(+/+)] mice. The responses were consistent among multiple end points. Airway responsiveness after methacholine challenge and bronchoalveolar lavage (BAL) fluid leukocyte and eosinophil numbers in TNFR(-/-) mice were equivalent or greater than those observed in TNFR(+/+) mice. Likewise, serum and BAL fluid IgE; lung interleukin (IL)-2, IL-4, and IL-5 levels; and lung histological lesion scores were comparable or greater in TNFR(-/-) mice compared with those in TNFR(+/+) mice. TNFR(+/+) mice chronically treated with anti-murine TNF antibody had BAL fluid leukocyte numbers and lung lesion scores comparable to control antibody-treated mice. These results suggest that, by itself, TNF does not have a critical proinflammatory role in the development of allergic inflammation in this mouse model and that the production of other cytokines associated with allergic disease may compensate for the loss of TNF bioactivity in the TNFR(-/-) mouse.
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21 MeSH Terms
TRF requirements for in vitro PFC responses to SRBC and R36a. I. TRF is distinct from IL 2 but indistinguishable from polyclonal BCSF.
Eisenberg L, Prystowsky MB, Dick RF, Sosman JA, Fitch FW, Quintáns J
(1984) J Immunol 132: 1305-10
MeSH Terms: Animals, Antibody-Producing Cells, Antigens, Bacterial, Antigens, T-Independent, B-Lymphocytes, Cell Line, Growth Substances, Hemolytic Plaque Technique, Interleukin-2, Interleukin-4, Interleukin-5, Isoantigens, Kinetics, Lymphocyte Depletion, Lymphokines, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Molecular Weight, Sheep, Streptococcus pneumoniae, T-Lymphocytes
Show Abstract · Added March 5, 2014
In vitro PFC responses to the thymus-independent (TI) antigen Streptococcus pneumoniae R36a require T cell replacing factor(s) (TRF). This requirement for TRF is as significant as for the thymus-dependent (TD) antigen SRBC. TRF is shown to be distinct from IL 2 by the following observations: 1) culture supernatants from the cloned T cell line L2, collected over an 8-day period after allogeneic stimulation, transiently contain IL 2 activity but maintain high levels of TRF activity throughout 192 hr; 2) L2V, a variant subclone of L2, produces much higher levels of TRF activity than the parental line but no detectable IL 2 activity; 3) the addition of IL2+, TRF- supernatants from the T cell hybridoma FS6-14.13 does not affect the L2V SF-driven PFC responses to R36a or SRBC; and 4) the addition of contaminating T cells to cultures containing T cell-depleted spleen cells, L2V SF, and antigen does not affect the PFC response. TRF does appear to be indistinguishable from polyclonal B cell stimulating factor (BCSF), which stimulates polyclonal PFC responses in the absence of antigen, mitogen, or anti-Ig. The TRF and BCSF activities of L2V SF could not be separated by ion-exchange, hydrophobic-interaction, and gel-filtration chromatography. TRF and BCSF have an apparent m.w. of approximately 40,000.
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22 MeSH Terms