Important note: Information in this article was accurate in 1998. The state of the art may have changed since the publication date.
Insulin selectively primes Th2 responses and induces regulatory tolerance to insulin in pre-diabetic mice.
Diabetologia. 1998 Feb;41(2):237-40. Unique Identifier : AIDSLINE MED/98158425 Tian J; Chau C; Kaufman DL; Department of Molecular and Medical Pharmacology, University of; California, Los Angeles 90095-1735, USA.
Abstract:
Little is known about the immunological impact of insulin administration other than it can boost insulin autoantibody levels. In particular, while the subcutaneous administration of a soluble foreign antigen (without adjuvant) is generally only weakly immunogenic in a naive animal, it is unknown what effect the subcutaneous administration of a soluble self-antigen has in animals with established autoimmune responses to the antigen. Addressing these questions in pre-diabetic nonobese diabetic NOD) mice, we examined the effects of administering insulin, as well as the metabolically inactive B-chain of insulin, on insulin-specific cellular and humoral immune responses. We show that pre-diabetic NOD mice have a spontaneous Th1-biased response against insulin. Administering insulin, or the insulin B-chain, rather than boosting the established Th1 response, primed Th2 cellular and humoral immunity to insulin, shifting the predominant insulin response toward a Th2 phenotype. Despite the presence of a Th1 response against insulin, insulin treated mice failed to mount proliferative T-cell responses following immunization and challenge with insulin, demonstrating that the treatment induced an active form of tolerance to this autoantigen. Thus, the subcutaneous administration of a soluble antigen can engage Th2 responses and induce self-tolerance, even after the establishment of autoreactive Th-1 responses. Such immune deviation and induced regulatory tolerance may contribute to the protective effects of prophylactic insulin therapy, as well as the establishment of a "honeymoon" phase in new-onset insulin-dependent diabetic patients.
Keywords: *Autoimmunity/IMMUNOLOGY *Diabetes Mellitus, Insulin-Dependent/IMMUNOLOGY *Insulin/IMMUNOLOGY *Th2 Cells/IMMUNOLOGY 980630
M9861759
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Important note: Information in this article was accurate in 1998. The state of the art may have changed since the publication date.
