Modulation of cellular-immune responses in vivo and in vitro by histamine receptor-bearing lymphocytes.

Rocklin, Ross E.

doi:10.1172/jci108347

Cited by 294 publications

(88 citation statements)

References 16 publications

(5 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Histamine has been shown to affect many aspects of lymphocyte functions, including proliferation (Wang & Zweiman, 1978;Beets & Dale, 1979;Brostoff, Pack & Lydyard, 1980;Ogden & Hill, 1980) and lymphokine production (Rocklin, 1976;Rocklin, Breard, Gupta, Good & Melmon, 1980), and this has led to the suggestion that endogenous histamine may act as an immunomodulator via an H2-receptor (Busse, 1979). However, this classification has been questioned by workers who found discrepancies between H2-receptor stimulating activity and inhibition of lymphocyte transformation (Beets & Dale, 1979;Vickers, Arlington, Jones, Martin & Melvin, 1980;Brostoff et al, 1980).…”

Section: Introduction Methodsmentioning

confidence: 99%

INHIBITION OF LYMPHOCYTE PROLIFERATION BY HISTAMINE AND RELATED COMPOUNDS NOT MEDIATED VIA H_1‐ OR H_2‐ RECEPTORS

Gordon

Lewis

Nouri

1981

British J Pharmacology

View full text Add to dashboard Cite

1 The effects of histamine and chemical analogues were examined on mitogen-stimulated human lymphocyte proliferation.2 Compounds with selective agonist activity at either Hl-or H2-receptors were found to inhibit proliferative responses, although N-3-methyl-histamine which does not act on either receptor was as inhibitory as histamine itself. 3 The H2-receptor agonist, dimaprit, had a profound inhibitory effect on proliferation, however nordimaprit, which has little or no H2-agonist activity, was more active on lymphocytes. Impromidine, although a potent H2-agonist, failed to produce such inhibition. 4 The effects of dimaprit and nordimaprit were not reversed by H2-receptor antagonists, cimetidine or metiamide. 5 These results do not support the view that the antiproliferative effects of histamine and related compounds are mediated via conventional Hl-or H2-receptors.6 SKF 93390 was found to be the most active of the dimaprit analogues tested, which could represent a novel series of potential immunosuppressive agents.

show abstract

Section: Introduction Methodsmentioning

confidence: 99%

INHIBITION OF LYMPHOCYTE PROLIFERATION BY HISTAMINE AND RELATED COMPOUNDS NOT MEDIATED VIA H_1‐ OR H_2‐ RECEPTORS

Gordon

Lewis

Nouri

1981

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…In a number of experimental systems in vitro, the activity of lymphoid cells was shown to be affected by treatment with histamine or histamine H2-receptor agonists/antagonists. These systems include antigen-or mitogen-induced lymphtocyte proliferation (Strannegard & Strannegard, 1977;Wang & Zweiman, 1978;Brostoff etal., 1980;Hebert et al, 1980;Ogden & Hill, 1980;Suzuki & Huchet, 1981), lymphocyte-mediated cytotoxicity in different systems (Plaut et al, 1975;Schwartz et al, 1980;1981), production of migration inhibition factor (Rocklin, 1976), and antibody production (Lima & Rocklin, 1981;Szewczuk, et al, 1981). Strannegard & Strannegard (1977) also showed that lymphocytes from atopic individuals are more sensitive to inhibition of PHA-induced thymidine incorporation by histamine than cells from normal individuals.…”

Section: Introductionmentioning

confidence: 99%

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H₂‐agents

Andersson¹,

Bergstrand²

1984

British J Pharmacology

View full text Add to dashboard Cite

Guinea‐pigs were sensitized to ovalbumin (OA) by immunization regimens chosen to cause antigen‐induced bronchial anaphylactic responses mediated mainly either by IgE‐like antibodies or by IgG1‐like antibodies. Treatment of the IgE‐producing animals for three weeks with the histamine H2‐receptor antagonist cimetidine (1 mg kg−1 i.p. once a day) or with the H2‐agonist dimaprit (0.1, 1.0, or 10 mg kg−1 i.p. once a day) led to a significantly reduced bronchial response capacity compared with that of the saline‐treated controls challenged intravenously with antigen one week after the end of treatment. The changes were biphasic and not strictly dose‐dependent. In contrast, acute treatment of immunized animals with a single dose of cimetidine (10 or 30 mg kg−1 i.v.) or dimaprit (1 or 10 mg kg−1 i.v.) 2 min before challenge with OA did not significantly affect the bronchial anaphylactic response. However, long‐term treatment with cimetidine (10 mg kg−1) or the dimaprit analogue, S‐[4‐(N, N‐dimethylamino)‐butyl] isothiourea (SKF Compound 91488) (1 mg kg−1), which is reported not to activate H2‐receptors, had no effect on the response capacity. Treatment with cimetidine (1 mg kg−1) or dimaprit (1 mg kg−1) did not influence the response capacity to antigen challenge in IgG1‐ type animals. Dimaprit (1 mg kg−1) did not affect the responsiveness to intravenous provocation with histamine in ‘IgE‐type’ animals. Antigen‐induced release of histamine from chopped lung tissue in vitro was not significantly affected in ‘IgE‐type’ animals treated with cimetidine (1 mg kg−1) or dimaprit (1 mg kg−1). Treatment of immunized animals with cimetidine or dimaprit one week before and one week after a booster injection of antigen also led to reduced response capacity compared with that of saline‐treated controls. However, the serum levels of IgE‐like homocytotropic antibodies of these animals were not reduced; on the contrary, those of IgG1‐antibody were increased in dimaprit‐treated animals. These data show that intermittent treatment with histamine H2‐agents reduces reagin‐mediated anaphylactic response capacity in vivo in actively sensitized guinea‐pigs by an as yet undefined mode of action.

show abstract

“…There have been reports showing that vasoactive amines can, under some conditions, reduce cell-mediated responses and could serve as a regulatory mechanism to limit responses (15,16). However, regardless of the actual role of vasoactive amines in conta.ct sensitivity, the present study shows that mice can produce reagin during contact sensitivity and therefore produce a strong cytotrophic antibody capable of arming the basophils present in contact hypersensitivity reactions.…”

Section: Discussionmentioning

confidence: 46%

Reaginic antibody produced in mice with contact sensitivity.

Thomas¹,

Asherson²,

Watkins³

1976

The Journal of Experimental Medicine

View full text Add to dashboard Cite

There has been some speculation that the T-cell-dependent contact hypersensitivity reactions contain elements of both immediate and delayed hypersensitivity. This has been provoked by the finding that the swelling reactions of contact sensitivity can be detected as early as 4 h after challenge (1) and by the demonstration that basophils constitute a significant proportion of the inflammation in contact sensitivity (2). Also lymphocytes have been shown to release a product capable of giving peritoneal exudate cells the ability to passively transfer contact sensitivity (3). The capacity of the sensitized peritoneal cells to passively transfer contact sensitivity was abrogated by treatment with antiimmunoglobulin sera. Askenase (4) has also reported that serum from mice painted with oxazolone can transfer a basophil inflammation when recipient mice were challenged 2 h after serum transfer. This reaction required 24 h after challenge to develop.More recently the possible contribution of immediate hypersensitivity reactions in contact sensitivity was emphasized by the investigation of Gershon et al. (5) who found that skin sites where contact sensitivity reactions are most easily elicited are particularly rich in mast cells. In addition mice with mast cells depleted of 5-hydroxytryptamine by reserpine could not manifest delayed hypersensitivity reactions although they had sensitized cells capable of passively transferring delayed hypersensitivity to normal recipients. They also showed that serum from mice repeatedly painted with oxazolone could produce a passive cutaneous anaphylaxis reaction in mice if challenged within 2 h of intradermal transfer. This early reaction in mice has been attributed to weak IgG homocytotrophic antibody (6). This communication shows that mice can produce reaginic antibody within a week of sensitization with contact sensitizing agents and therefore have a strong homocytotrophic antibody capable of arming the basophils in contact sensitivity reactions. The reaginic antibody was unusual in that it was elicited by large doses of antigen without adjuvant and could be boosted by repeated challenge. Materials and MethodsMice. 6-to 12-wk-old mice bred at the Clinical Research Centre were used. Application of Picryl Chloride and Oxazolone. Mice were shaved on the thorax and abdomen and usually painted with either 0.1 ml of 5% picryl chloride (BDH, Poole, Dorset, Great Britain) or 0.1 ml of 3% oxazolone (2-phenyl-4-ethoxymethylene oxazolone) (Sigma Chemical Co., St. Louis, Mo.) on the shaven areas and forepaws. The contact sensitizers were dissolved in ethanol just before application.

show abstract

Modulation of cellular-immune responses in vivo and in vitro by histamine receptor-bearing lymphocytes.

Cited by 294 publications

References 16 publications

INHIBITION OF LYMPHOCYTE PROLIFERATION BY HISTAMINE AND RELATED COMPOUNDS NOT MEDIATED VIA H_1‐ OR H_2‐ RECEPTORS

INHIBITION OF LYMPHOCYTE PROLIFERATION BY HISTAMINE AND RELATED COMPOUNDS NOT MEDIATED VIA H_1‐ OR H_2‐ RECEPTORS

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H₂‐agents

Reaginic antibody produced in mice with contact sensitivity.

Contact Info

Product

Resources

About

Modulation of cellular-immune responses in vivo and in vitro by histamine receptor-bearing lymphocytes.

Cited by 294 publications

References 16 publications

INHIBITION OF LYMPHOCYTE PROLIFERATION BY HISTAMINE AND RELATED COMPOUNDS NOT MEDIATED VIA H1‐ OR H2‐ RECEPTORS

INHIBITION OF LYMPHOCYTE PROLIFERATION BY HISTAMINE AND RELATED COMPOUNDS NOT MEDIATED VIA H1‐ OR H2‐ RECEPTORS

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H2‐agents

Reaginic antibody produced in mice with contact sensitivity.

Contact Info

Product

Resources

About

INHIBITION OF LYMPHOCYTE PROLIFERATION BY HISTAMINE AND RELATED COMPOUNDS NOT MEDIATED VIA H_1‐ OR H_2‐ RECEPTORS

INHIBITION OF LYMPHOCYTE PROLIFERATION BY HISTAMINE AND RELATED COMPOUNDS NOT MEDIATED VIA H_1‐ OR H_2‐ RECEPTORS

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H₂‐agents