| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
From the Section of Comparative Medicine and Departments of Medicine and Pathology, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06510
Abstract
In previous work monoamine depletion due to treatment with reserpine was shown to decrease the elicitability of DTH responses in mice. In addition, treatment with monoamine oxidase inhibitors prevented the reserpine-induced decrease. These findings led to the suggestion that serotonin-induced increased vascular permeability is necessary to the development of DTH reactions, perhaps by allowing bone marrow-derived macrophage precursor cells, which are obligate components of DTH responses, to migrate through specialized venules into the site of the reaction. We have compared classical drug tachyphlaxis (temporary inhibition of the effects of a drug by prior treatment with agonists) to serotonin in vessels of mouse feet with local inhibition of DTH after serotonin pretreatment of mice. During the tachyphylactic period, DTH responses are depressed. This suggests that serotonin-induced tachyphylaxis of local endothelial receptors can be responsible for DTH inhibition. In contrast, local injection of histamine has no effect on DTH and this drug is a much less potent inducer of tachyphylaxis to serotonin-mediated vasoactive reactions. On the other hand, histamine can inhibit in vitro T cell reactions, which are not affected by serotonin. These data help to further the concept that serotonin plays an important role in the regulation of DTH in mice and that it probably does so by acting on vascular endothelium.
Footnotes
1 This work was supported in part by United States Public Health Service Grants CA 08593, AI-10497, CA-14216, AI-12211, AI-11707, and from the American Cancer Society Grant IM-70B.
2 Allergic Disease Academic Awardee AI-70829.
This article has been cited by other articles:
|
|
 |
|
  P. W. Askenase, A. Itakura, M. C. Leite-de-Moraes, M. Lisbonne, S. Roongapinun, D. R. Goldstein, and M. Szczepanik TLR-Dependent IL-4 Production by Invariant V{alpha}14+J{alpha}18+ NKT Cells to Initiate Contact Sensitivity In Vivo J. Immunol., November 15, 2005; 175(10): 6390 - 6401. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. A. Campos, M. Szczepanik, A. Itakura, M. Akahira-Azuma, S. Sidobre, M. Kronenberg, and P. W. Askenase Cutaneous Immunization Rapidly Activates Liver Invariant V{alpha}14 NKT Cells Stimulating B-1 B Cells to Initiate T Cell Recruitment for Elicitation of Contact Sensitivity J. Exp. Med., December 15, 2003; 198(12): 1785 - 1796. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Szczepanik, M. Akahira-Azuma, K. Bryniarski, R. F. Tsuji, I. Kawikova, W. Ptak, C. Kiener, R. A. Campos, and P. W. Askenase B-1 B Cells Mediate Required Early T Cell Recruitment to Elicit Protein-Induced Delayed-Type Hypersensitivity J. Immunol., December 1, 2003; 171(11): 6225 - 6235. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Akiba, J. Kehren, M.-T. Ducluzeau, M. Krasteva, F. Horand, D. Kaiserlian, F. Kaneko, and J.-F. Nicolas Skin Inflammation During Contact Hypersensitivity Is Mediated by Early Recruitment of CD8+ T Cytotoxic 1 Cells Inducing Keratinocyte Apoptosis J. Immunol., March 15, 2002; 168(6): 3079 - 3087. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. F. Tsuji, I. Kawikova, R. Ramabhadran, M. Akahira-Azuma, D. Taub, T. E. Hugli, C. Gerard, and P. W. Askenase Early Local Generation of C5a Initiates the Elicitation of Contact Sensitivity by Leading to Early T Cell Recruitment J. Immunol., August 1, 2000; 165(3): 1588 - 1598. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
