Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P14784 (
IL-2 receptor
)
3,849
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The ability of adherent and nonadherent peripheral blood mononuclear cells (PBMC) from forty patients with
schistosomiasis
to produce IL-1 and IL-2 was studied. The results indicated that ConA-stimulated nonadherent-PBMC from patients exhibited a decreasing ability to produce IL-2 compared with controls (P less than 0.001), and that their ConA-activated blast cells expressed a smaller number of cell surface
IL-2 receptor
since IL-2 adsorption to the patient cells was lower than that to the normal cells (P less than 0.01). On the other hand, IL-1 production by LpS-stimulated adherent-PBMC from the patients was in agreement with that from the normal controls (P greater than 0.05). From above results, it seems that human organism following infection of Schistosoma japonicum might display a sort of suppressive phenomenon in the production of and the response to IL-2.
...
PMID:[Observation on the production of interleukin-1 and interleukin-2 and response to interleukin-2 in patients with schistosomiasis]. 190 57
Anti-idiotypic (anti-Id) T cells from
schistosomiasis
patients or former patients proliferate upon exposure to polyclonal or monoclonal anti-soluble egg antigen (SEA) antibodies. Chloroquine does not inhibit, the response, which is induced by F(ab')2 (but not soluble Fab) fragments of these antibodies. Purified T cells from former patients require macrophages or exogenous IL-1 to respond to anti-SEA Ids and can respond to matrix-bound Fab fragments in the presence of IL-1. These anti-Id T cells recognize the Ids directly. Chronic
schistosomiasis
patients immunoregulate the production of a non-IL-2 lymphokine that stimulates
IL-2 receptor
expression on resting T cells. This regulation is reversed upon chemotherapeutic cure.
...
PMID:Immunoregulation in human schistosomiasis by idiotypic interactions and lymphokine-mediated mechanisms. 315 Oct 84
Granulomatous tissue reactions appear in athymic mouse skin, indicating that initiation of granuloma formation may be T-cell independent. To further evaluate the relationships between granuloma formation and T-cell function, we treated euthymic BALB/c mice with cyclosporine (Cs), a potent immunosuppressive drug, injected intramuscularly (150 mg/kg/day) 5 times a week. Hepatic granulomas were isolated from mice with
schistosomiasis
and transplanted into the skin of mice treated with Cs for 2 weeks. Cyclosporine injection was continued for 3 additional weeks. Blood levels of the drug increased during treatment (489 ng/ml at 2 weeks and 822 ng/ml at 5 weeks). Morphologically identical granulomas developed in both treated and untreated mice. Examination for T-cell functions showed that by the end of 2 weeks treatment, concanavalin A, phytohemagglutinin responses, and IL-2 activity were markedly depressed, and
IL-2 receptor
expression was not detected in either lymph nodes or spleen of the Cs-treated mice; however, after hepatic granuloma graft, T-cell functions in regional lymph nodes, but not in spleen, as well as peripheral blood eosinophilia were stimulated in Cs-treated mice. These data strongly suggest that intact T-cell activity is not essential for the initiation of granuloma formation. In addition, granuloma grafts appear to stimulate Cs-resistant T-cell activation locally, which amplifies and organizes the granulomatous response.
...
PMID:Skin granuloma formation in mice immunosuppressed by cyclosporine. 335 30
Schistosomiasis
causes pathology in an estimated 200 million individuals. Clinical disease is caused by a complex immunopathologic response to the parasite ova, which are deposited in the host tissues. This immunopathologic response is caused by T lymphocytes which express the high-affinity
IL-2 receptor
(IL-2R). DAB389IL-2 is a diphtheria toxin-IL-2 fusion toxin protein which functionally inactivates or kills cells which bear the high-affinity IL-2R. DAB389IL-2 has been used in man to suppress IL-2R-dependent immune reactivity. Therefore, we reasoned that DAB389IL-2 might suppress immunopathology in
schistosomiasis
. In these studies we assessed the in vitro and in vivo effects of DAB389IL-2 on the development of immunopathology in murine
schistosomiasis
. DAB389IL-2 suppressed IL-2, lectin mitogen (Con A), and soluble Schistosoma mansoni egg antigen-induced lymphocyte proliferation and in vitro granuloma formation. In addition, DA-B389IL-2 suppressed in vitro IL-2R expression. DA-B389IL-2 also suppressed the development of granulomas and collagen deposition in vivo in the livers of infected animals. Therefore, DAB389IL-2 may have potential for the targeted reduction of immunopathology due to
schistosomiasis
in man.
...
PMID:Suppression of immunopathology in schistosomiasis by interleukin-2-targeted fusion toxin, DAB389IL-2. I. Studies of in vitro and in vivo efficacy. 749 23