Transfer of an antigen-specific immediate hypersensitivity-like reaction with an antigen-binding factor produced by T cells.

Ptak, W; Askenase, Philip W.; Rosenstein, Robert W.; Gershon, Richard K.

doi:10.1073/pnas.79.6.1969

Cited by 23 publications

(19 citation statements)

References 15 publications

(12 reference statements)

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“…Subsequently, it has been shown that mononuclear cells, lymphocytes, and pulmonary macrophages produce histamine-releasing factors (HRF)' that activate human mast cells and basophils with increased di-rected migration and release of histamine and leukotrienes (5)(6)(7)(8)(9). Another group of lymphokines has been identified in rodents that specifically binds to antigens and releases serotonin from mast cells (10). Thus, it is apparent that immunoregulatory cells produce a number of substances that stimulate the growth and function of mast cells and basophils.…”

Section: Introductionmentioning

confidence: 99%

Identification of a histamine release inhibitory factor produced by human mononuclear cells in vitro.

Alam

Lett-Brown

1988

J. Clin. Invest.

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Human mononuclear cells (MNC) secrete histamine-releasing factor(s) (HRF) when cultured in vitro. HRF induces the release of histamine and other mediators from basophils and mast cells. We have shown that MNC also produce a histamine release inhibitory factor (HRIF), and that the synthesis is augmented by culture with physiologic concentrations of histamine (10-10 to 10' M) and by the mitogen concanavalin A (Con A). HRIF does not affect release initiated by other secretagogues such as allergen, anti-IgE, C5a, Con A, and phorbol myristate acetate. HRIF requires a preincubation with the cells for 5-10 min for maximal inhibition, and this effect is not abolished by washing the cells after the preincubation. The biological activity of HRIF is protease-sensitive, neuraminidase-resistant, and relatively heat-stable. HRIF can be distinguished from HRF by a lower apparent molecular mass (8,000-10,000 D).

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Section: Introductionmentioning

confidence: 99%

Identification of a histamine release inhibitory factor produced by human mononuclear cells in vitro.

Alam

Lett-Brown

1988

J. Clin. Invest.

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“…The fact that DTH reactions depend on T cell activation of local mast cells led us to search for factors that might mediate T ceil activation of mast cells. Such a factor has been described recently (6,7). It is a T cell-derived antigenbinding factor that transfers an antigen-specific immediate hypersensitivity-like reaction (6).…”

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confidence: 99%

“…Such a factor has been described recently (6,7). It is a T cell-derived antigenbinding factor that transfers an antigen-specific immediate hypersensitivity-like reaction (6). The T cell factor has in vivo activity analogous to IgE antibody, but can be distinguished from IgE by a number of immunochemical and biological properties (6,7).…”

mentioning

confidence: 99%

“…It is a T cell-derived antigenbinding factor that transfers an antigen-specific immediate hypersensitivity-like reaction (6). The T cell factor has in vivo activity analogous to IgE antibody, but can be distinguished from IgE by a number of immunochemical and biological properties (6,7). Importantly, the T cell factor, like IgE, is mast cell dependent, since neither transfer the ability to elicit skin reactions in mast cell-deficient W/W v or SI/S1 d mice.…”

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confidence: 99%

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An early component of delayed-type hypersensitivity mediated by T cells and mast cells.

Loveren¹,

Meade²,

Askenase³

1983

The Journal of Experimental Medicine

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142

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In four different systems it was shown that murine delayed-type hypersensitivity (DTH) responses at 18-48 h were preceded by early 2-h responses. CBA mice immunized with picryl chloride, BDF1 mice immunized with oxazolone, BALB/c mice immunized with dinitrofluorobenzene, and C57BL/6 mice immunized with L5178Y lymphoma cells, and challenged with the appropriate specific antigen, all gave rise to expected 18-48 h delayed-in-time hypersensitivity reactions, but all of these responses were preceded by early hypersensitivity reactions that peaked at 2 h. These early 2-h reactions are transferable with T cells or with a T cell-derived, antigen-binding factor and are antigen-specific. The early and late components of DTH reactions are mast cell dependent since neither are elicited in mast cell deficient W/Wv or Sl/Sld mice. The T cell activity mediating the early component of DTH is demonstrable as early as 24 h after immunization, while the classical late component of DTH is not demonstrable until days 3-4. The difference in onset after immunization of the early and late components of DTH, and the different kinetics of these components in recipients of cell transfers that were challenged immediately or 24 h after transfer, led to the hypothesis that immunization for DTH leads to rapid induction in lymphoid organs of a certain population of T cells to produce an antigen-binding factor. This factor sensitizes peripheral tissues, probably mast cells, and local challenge with appropriate antigen leads to mast cell activation and release of the vasoactive amine serotonin, resulting in increased permeability of the local vasculature. This allows other circulating antigen-specific T cells, which are induced later after immunization, to enter the tissues and interact with antigen, resulting in production of chemoattractant lymphokines that recruit accessory leukocytes such as monocytes and polymorphs to enter the tissues via gaps between endothelial cells. These inflammatory cells, that are recruited to the site via two different T cell activities, constitute the characteristic infiltrate of DTH responses. Identification of an early 2-h component of DTH that is T cell- and mast cell-dependent provides evidence that the tissue-sensitizing, antigen-binding, T cell factor probably functions in vivo in the early phases of DTH responses.

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“…Active systemic anaphylaxis may thus develop in mice lacking IgE [4]. Ptak et al [5]have further demonstrated that antigen–binding T cell factors, released from T cells of immunized mice, have the capacity to transfer to naive mice the ability to mount an antigen–specific immediate hypersensitivity–like reaction following challenge with antigen [5, 6]. These T cell factors bind to receptors on the surface of mast cells and induce the release of mediators after challenge with antigen [7].…”

Section: Introductionmentioning

confidence: 99%

Lack of Systemic Anaphylaxis and Aeroallergen–Induced Airway Plasma Extravasation in Allergic Immunoglobulin–Deficient Mice

Korsgren

Erjefält

Korsgren

et al. 1999

Int Arch Allergy Immunol

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Background: In Ig–deficient mice allergen challenge–induced pulmonary late phase inflammation is at least as pronounced as in wild–type animals. This study investigates immediate hypersensitivity responses in these mice. Methods: To examine the acute plasma extravasation response in airway tissue, immunized Ig–deficient and wild–type mice and sham–immunized wild–type controls were subjected to 15 min ovalbumin aerosol challenge. 125I–albumin was injected (i.v.) 1 min prior to challenge. Immediately after challenge 131I–albumin was injected and the experiment was terminated. Plasma and trachea were analyzed for 125I and 131I, and the amount of extravasated plasma in the trachea was calculated. To study the development of systemic anaphylaxis immunized Ig–deficient and wild–type animals recieved intravenous allergen challenge followed by determination of mast cell responses and plasma histamine levels. Results: Allergen aerosol–exposed immunized wild–type mice exhibited marked plasma extravasation in the trachea (pd0.01 vs. wild–type controls), but in the corresponding Ig–deficient mice there was no increased extravasation. Immunized Ig–deficient mice receiving intravenous allergen challenge were resistant to anaphylactic shock. By contrast, the wild–type animals developed systemic anaphylaxis, accompanied by plasma extravasation, mast cell degranulation, elevated plasma histamine and rapid death. Conclusion: The present data are evidence that immunoglobulins are crucial for the development of immediate (type 1) responses. These findings together with our previous observations on late–phase pulmonary responses suggest that immediate hypersensitivity processes are unimportant for development of the late phase inflammation in the respiratory tract of mice.

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Transfer of an antigen-specific immediate hypersensitivity-like reaction with an antigen-binding factor produced by T cells.

Cited by 23 publications

References 15 publications

Identification of a histamine release inhibitory factor produced by human mononuclear cells in vitro.

Identification of a histamine release inhibitory factor produced by human mononuclear cells in vitro.

An early component of delayed-type hypersensitivity mediated by T cells and mast cells.

Lack of Systemic Anaphylaxis and Aeroallergen–Induced Airway Plasma Extravasation in Allergic Immunoglobulin–Deficient Mice

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