Effect of sera from immunologically altered mice on phytohemagglutinin‐induced mouse lymphocyte transformation

Nelson, David S.; Penrose, Jean M.; Shneider, Cynthia N.

doi:10.1002/eji.1830061018

Cited by 5 publications

(2 citation statements)

References 23 publications

(5 reference statements)

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“…In many human diseases serum from patients either fails adequately t o support, or inhibits, lymphocyte transformation [2-41. For example, normal human lymphocytes respond less well to PHA [3, 51, mitogens [6] or allogeneic lymphocytes [7] in the presence of serum from patients with leprosy than in normal human serum. Uremic serum or plasma actively inhibits the response of normal human lymphocytes t o PHA [8,9].…”

Section: Introductionmentioning

confidence: 99%

Effect of normal mouse serum on mouse lymphocyte transformation in vitro

Nelson

Shneider

1974

Eur J Immunol

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Mouse spleen cells were cultured in the presence or absence of one of the following mitogens: phytohemagglutinin (PHA), concanavalin A, allogeneic spleen cells or bacterial lipopolysaccharide. The addition of normal mouse serum (NMS) to the cultures usually depressed mitogen-induced lymphocyte transformation as measured by DNA, RNA o r protein synthesis, whether calculated as gross o r net synthesis. The degree of depression was increased as the concentration of NMS serum increased. DNA and RNA synthesis in unstimulated cultures were also usually depressed by NMS. NMS added 24 hours or more after the start of cultures with PHA o r allogeneic lymphocytes was less depressive than serum present from the start and in some cases, actually increased DNA synthesis. The presence of NMS in cultures containing supra-optimal doses of concanavalin A could also increase DNA synthesis. Cells incubated with NMS for 2 4 hours survived as well as cells incubated without NMS, but subsequently responded less well t o PHA. Cells passed through a column of glass wool had a lower baseline DNA synthesis, which was not inhibited by NMS; they responded less well to mitogens and this response was further depressed by NMS.It is suggested that NMS contains a factor which damps the proliferation of mouse T and B cells, without exerting an overt cytotoxic effect, and that it acts directly on lymphocytes.

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Section: Introductionmentioning

confidence: 99%

Effect of normal mouse serum on mouse lymphocyte transformation in vitro

Nelson

Shneider

1974

Eur J Immunol

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“…It has been shown that patients with Virchowian hanseniasis (COCHRANE & SMYLY, 1964;RABELLO JR., 1938;RABELLO JR. & AZULAY, 1975;ROTBERG, 1937) present a deficit of. cell mediated immunity (CMI) (BLADEN, 1974;BULLOCK JR., 1968CONVIT et a/., 1971;GODAL, 1978;MACKANESS & BLADEN, 1967;MILLER & OSOBA, 1967;NELSON, 1974;NELSON et al, 1971;NORTH, 1973;SER. INF.…”

Section: Introductionmentioning

confidence: 99%

Cell mediated immunity in patients with virchowian hanseniasis before and after treatment with transfer factor

LESER,

MARGARIDO,

BELDA

et al. 1980

Hansen. Int.

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Cell mediated immunity (CMI), bacterial index (BI), morphological index (MI), skin and lymph nodes biopsies were evaluated in 15 patients with virchowian hanseniasis before and after treatment with transfer factor (TF) obtained from human spleens. The patients were divided in 3 groups: group I (control) received only sulforiti, group II received sulfone plus TF and group III received only TF. There was no difference in the numbers of peripherical T and B lymphocytes of patients and normal controls. Before the treatment with TF, there was an impaired response of the patient's peripheral lymphocytes to PHA stimulus, in the presence of autologous or homologous plasma. This depressed response was corrected after treatment With TF in the patients of group III. In none of the patients a positive Mitsuda reaction was observed before and after treatment with TF. The improvement of the MI observed in group IH, treated only with TF was remarkably similar to the patients treated only with sulfone. This work points out that TF has a role in the treatment of patients with virchowian hanseniasis, based on the improvement of CMI, MI, on histopathology of skin biopsies and clinical conditions.

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Tolerance in rats by transplacental transfer of Dipetalonema viteae microfilariae: recognition of putative tolerogen(s) by antibodies that inhibit antigen‐Specific lymphocyte proliferation

et al. 1988

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We have previously reported (Nature 1982. 299:361) that the transplacental transfer of Dipetalonema viteae microfilariae (mf) can induce an antigen-specific tolerance in rats. Rats thus tolerized have serum factor(s) which block(s) antigen-specific lymphocyte proliferation. The results of experiments involving fractionation of antisera from tolerant animals indicate that the inhibitory activity for antigen-specific blastogenesis resides in IgG antibodies. Absorption of IgG (eluted from protein A) with specific filarial antigens reduced the inhibition from 58% to 9% whereas a similar immunosorption of IgG size fraction (obtained by applying to AcA 34 Ultrogel) resulted in a decrease from 72% to 35%. This suggests that IgG size fraction might include factor(s) derived from mf and was partially blocking the blastogenic response. Since the tolerant animals harbor only mf, we have used radiolabeled mf surface antigens for immunoprecipitation by antisera from tolerant animals. Antibodies from tolerant animals have a different specificity for filarial antigens compared to those from immunocompetent and mf-resistant rats.

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Effect of sera from immunologically altered mice on phytohemagglutinin‐induced mouse lymphocyte transformation

Cited by 5 publications

References 23 publications

Effect of normal mouse serum on mouse lymphocyte transformation in vitro

Effect of normal mouse serum on mouse lymphocyte transformation in vitro

Cell mediated immunity in patients with virchowian hanseniasis before and after treatment with transfer factor

Tolerance in rats by transplacental transfer of Dipetalonema viteae microfilariae: recognition of putative tolerogen(s) by antibodies that inhibit antigen‐Specific lymphocyte proliferation

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