Title

Cell-Mediated Immunity and Rat Pulmonary Late Allergic Responses [abstract]

Document Type

Article

Language

eng

Format of Original

1 p.

Publication Date

1-1993

Publisher

Elsevier

Source Publication

Journal of Allergy and Clinical Immunology

Source ISSN

0091-6749

Original Item ID

Shelves: RC583 .J Memorial Periodicals

Abstract

We have previously reported that the formation of antigen-specific IgE antibody in rats is associated with the induction of immediate but no late changes (airway inflammation and increased resistance) following pulmonary antigen challenge. Rats sensitized to dinitrophenol (DNP)-ovalbumin (OA) develop IgE and IgG anti-DNP antibodies and isolated immediate but no late responses when challenged with DNP-BSA; in contrast, only IgG anti-OA is simultaneously produced and OA challenge results in mild immediate and substantial late pulmonary reactions. To determine if cell-mediated immune responses may also be relevant to these observed differences in responses, we measured in vitro lymphocyte proliferative responses to DNP-BSA, OA, and concanavalin A (Con A) in both sensitized and control rats. Splenic and blood lymphocytes were cultured with varying concentrations of antigen (0.5, 5, 50, 500 µg/ml), pulsed with 1 % tritiated thymidine on day 3 or 7, and counted 8 hours later. Cells obtained from sensitized rats developed dose-dependent response to OA (P<.0001) but no significant response to DNP-BSA. Cells from control rats did not response to either OA or DNP-BSA. DNP-BSA did not decrease OA-induced responses, indicating no toxic effect on the prolierative response. Since the pattern of in vitro lymphocyte proliferative response to antigen parallels the presence or absence of a late reaction in vivo with the same antigen, our results indicate that sensitized lymphocytes contribute to the cellular and physiologic alterations that occur during the late reaction in this species.

Comments

Journal of Allergy and Clinical Immunology, Vol. 91, No. 1, Part 2 (January 1993): 238. Publisher Link.

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