T cells produce an antigen-binding factor with in vivo activity analogous to IgE antibody.

Askenase, Philip W.; Rosenstein, Robert W.; Ptak, W

doi:10.1084/jem.157.3.862

Cited by 79 publications

(36 citation statements)

References 21 publications

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“…We propose that separated L chains, exclusive of H chains, may act directly by binding to postulated receptors on mast cells (11,13,14,24), since L chain-mediated CS initiation was shown in this study (Fig. 5, b and c) to be C-independent while being mast cell-dependent (Fig.…”

Section: Discussionmentioning

confidence: 94%

Subunits of IgM Reconstitute Defective Contact Sensitivity in B-1 Cell-DeficientxidMice: κ Light Chains Recruit T Cells Independent of Complement

Paliwal

Tsuji

Szczepanik

et al. 2002

The Journal of Immunology

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The elicitation of contact sensitivity (CS) to local skin challenge with the hapten trinitrophenyl (TNP) chloride requires an early process that is necessary for local recruitment of CS-effector T cells. This is called CS initiation and is due to the B-1 subset of B cells activated at immunization to produce circulating IgM Ab. At challenge, the IgM binds hapten Ag in a complex that locally activates C to generate C5a that aids in T cell recruitment. In this study, we present evidence that CS initiation is indeed mediated by C-activating classic IgM anti-TNP pentamer. We further demonstrate the involvement of IgM subunits derived either from hybridomas or from lymphoid cells of actively immunized mice. Thus, reduced and alkylated anti-TNP IgM also initiates CS, likely due to generated H chain-L chain dimers, as does a mixture of separated H and L chains that still could weakly bind hapten, but could not activate C. Remarkably, anti-TNP κ L chains alone mediated CS initiation that was C-independent, but was dependent on mast cells. Thus, B-1 cell-mediated CS initiation required for T cell recruitment is due to activation of C by specific IgM pentamer, and also subunits of IgM, while κ L chains act via another C-independent but mast cell-dependent pathway.

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Section: Discussionmentioning

confidence: 94%

Subunits of IgM Reconstitute Defective Contact Sensitivity in B-1 Cell-DeficientxidMice: κ Light Chains Recruit T Cells Independent of Complement

Paliwal

Tsuji

Szczepanik

et al. 2002

The Journal of Immunology

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“…The lymphocyte and the mast cell are two key inflammatory cells in the non-atopic reactions in the mouse airways as well as the skin and the intestine (7,30,31). In skin studies, it has been demonstrated that, upon contact sensitization, B lymphocytes are activated to produce hapten-specific immunoglobulin kappa light chains (IgLC) in spleen and lymph nodes (32).…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms involved in the induction and ongoing respiratory impairments associated with non-atopic asthma are poorly investigated (2). It has become apparent that non-IgE-mediated cell-mediated reactions can occur in the airways (6)(7)(8) of sensitized animals after local challenge with low molecular weight compounds. These reactions in the lung are not mediated by IgE.…”

Section: Introductionmentioning

confidence: 99%

Murine Model for Non-IgE-Mediated Asthma

et al. 2004

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Abstract-There is increasing evidence that inflammatory mechanisms other than atopy or eosinophilic inflammation may be involved in the pathogenesis of asthma. The mechanisms associated with non-atopic (non-IgE) or neutrophil-mediated asthma are poorly investigated. Nonatopic airway inflammation and hyperresponsiveness was induced in mice by skin sensitization with dinitrofluorobenzene (DNFB) followed by intra-airway challenge with dinitrobenzene sulfonic acid (DNS). Acute bronchoconstriction and mast cell activation were observed shortly after challenge. Increased levels of the major mast cell mediator, TNF-α, were found in the bronchoalveolar lavage fluid of DNFB-sensitized. Mast cells play a key role in the early release of TNF-α since mast-celldeficient WBB6F 1 -W/W V mice did not show an increase in TNF-α release after DNFB-sensitization and DNS challenge compared to their ++ littermates. Features of the late-phase pulmonary reaction included mononuclear and neutrophilic cell infiltration, pulmonary edema, in vitro tracheal hyperreactivity and in vivo airway hyperresponsiveness. These characteristics bear marked similarity with those observed in non-atopic asthmatic patients. Therefore, this model can be used to further study the mechanisms potentially responsible for the development of non-IgE-mediated asthma.

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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).…”

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.…”

mentioning

confidence: 99%

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

Loveren¹,

Meade²,

Askenase³

1983

The Journal of Experimental Medicine

Self Cite

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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T cells produce an antigen-binding factor with in vivo activity analogous to IgE antibody.

Cited by 79 publications

References 21 publications

Subunits of IgM Reconstitute Defective Contact Sensitivity in B-1 Cell-DeficientxidMice: κ Light Chains Recruit T Cells Independent of Complement

Subunits of IgM Reconstitute Defective Contact Sensitivity in B-1 Cell-DeficientxidMice: κ Light Chains Recruit T Cells Independent of Complement

Murine Model for Non-IgE-Mediated Asthma

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

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