HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Doherty, P. C. Articles by Zinkernagel, R. M. Search for Related Content PubMed Articles by Doherty, P. C. Articles by Zinkernagel, R. M.

Capacity of Sensitized Thymus-Derived Lymphocytes to Induce Fatal Lymphocytic Choriomeningitis Is Restricted by the H-2 Gene Complex

Department of Microbiology, The John Curtin School of Medical Research, Canberra A.C.T., Australia

Abstract

Adoptive immunization of syngeneic, immunosuppressed recipients infected with lymphocytic choriomeningitis (LCM) virus causes fatal neurologic disease within 2 to 4 days of cell transfer, providing that donors are sampled when the in vitro ⁵¹Cr release assay shows maximal specific activity of sensitized thymus-derived lymphocytes (T cells). Prior treatment of immune spleen cells with AKR anti- ascitic fluid and complement causes total abrogation of this in vivo activity. Fatal neurologic disease is induced only when donor and recipient share at least one set of H-2 antigenic specificities. Parent F1 and F1 parent combinations are as effective as syngeneic systems, but mice given allogeneic immune cells survive as long as controls. Differences at the M-locus in H-2 compatible mice do not inhibit effector activity. Homing of transferred lymphocytes to spleen is similar in syngeneic or allogeneic recipients, but only syngeneic immune cells cross the blood-cerebrospinal fluid (CSF) barrier and cause choriomeningitis. Fatal LCM, is, therefore, apparently induced by a specifically sensitized -bearing cell population, activity of which is restricted by the H-2 gene complex.