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Invariant NKT Cells Rapidly Activated via Immunization with Diverse Contact Antigens Collaborate In Vitro with B-1 Cells to Initiate Contact Sensitivity¹

Regis A. Campos^*, Marian Szczepanik, Mariette Lisbonne, Atsuko Itakura, Maria Leite-de-Moraes and Philip W. Askenase^2,

^* Immunology Service of Professor Edgar Santos, Federal University of Bahia, Salvador-BA, Brazil; Department of Human Developmental Biology, Jagiellonian University College of Medicine, Krakow, Poland; Section of Allergy and Clinical Immunology, Department of Medicine, Yale University School of Medicine, New Haven, CT 06520; and Centre National de la Recherche Scientifique Unité Mixte de Recherche 8147, Paris V, Hôpital Necker, Paris, France

In cutaneous contact sensitivity there is an early elicited innate cascade of complement, mast cells, and platelets activated via IgM Abs. This response is required to initiate the elicitation of acquired classical contact sensitivity by leading to local recruitment of effector T cells. We recently performed in vivo experiments showing that collaboration is required between innate-like invariant V14⁺ NKT cells (iNKT) and the innate-like B-1 B cell subset to induce this initiation process. Contact sensitization triggers iNKT cells to produce IL-4 to coactivate the B-1 cells along with specific Ag for production of the initiating IgM Abs. We now describe in vitro collaboration of iNKT and B-1 cells. Normal peritoneal B-1 cells, incubated in vitro with soluble Ag, and with 1-h in vivo immune iNKT cells producing IL-4, are activated to mediate the contact sensitivity-initiation cascade. The three components of this process can be activated by different Ag. Thus, 1-h iNKT cell activation, B-1 cell stimulation, and generation of immune effector T cells can be induced by sensitization with three different Ag to respectively generate IL-4 and Ag-specific IgM Abs, to recruit the Ag-specific effector T cells. These findings have relevance to allergic and autoimmune diseases in which infections can trigger exacerbation of T cell responses to allergens or to autoantigens.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by funds from the National Institutes of Health, AI-59801 and AI-07174 (to P.W.A.); the Centre National de la Recherche Scientifique and Fondation pour la Recherche Médicale (to M.L.-d.-M.); the Polish Committee of Scientific Research (to M.S.); and a Fugisawa grant from the Academy of Allergy, Asthma and Immunology, and Programa de Fixação de Doutores no Estado da Bahia-Fundação de Amparo à Pesquisa do Estado da Bahia from the State of Bahia, Brazil (to R.A.C.).

² Address correspondence and reprint requests to Dr. Philip W. Askenase, Section of Allergy and Clinical Immunology, Department of Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8013. E-mail address: philip.askenase{at}yale.edu

³ Abbreviations used in this paper: CS, contact sensitivity; -GalCer, -galactosylceramide; iNKT, invariant NKT; LMNC, liver mononuclear cell; OX, oxazolone; TNP, trinitrophenol; TNP-Cl, TNP chloride, picryl chloride.

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