Neonatal Thymectomy Results in a Repertoire Enriched in T Cells Deleted in Adult Thymus

Abstract

In B6AF1 mice, T lymphocytes that use the V beta 11-positive (and not V beta 6-positive or V beta 8-positive) segment in their receptor for antigen are greatly reduced in the thymus and peripheral lymphoid tissues, most likely as a result of clonal deletion. The relative number of V beta 11-positive cells in adult lymph nodes was ten times as high in B6AF1 mice thymectomized 1 to 4 days after birth as in normal mice. Moreover, for the first 10 days of life of B6AF1 mice, mature V beta 11-positive T cells were readily detected in the thymus and spleen. Thus neonatal thymectomy results in the maintenance of the receptor repertoire of early postnatal life, and this correlates with the subsequent development of organ-specific autoimmune diseases.

Cutting Edge: Autoimmune Disease in Day 3 Thymectomized Mice Is Actively Controlled by Endogenous Disease-Specific Regulatory T Cells

“…The first hypothesis was supported by the finding of T cell responses to endogenous mouse mammary tumor virus (MMTV) superantigen (8). Thymic expression of endogenous MMTV superantigen in B6AF1 mice appeared late in ontogeny, and the deletion of cognate V␤11 ϩ CD4 ϩ CD8 Ϫ thymic or peripheral T cells was not observed until neonatal day 10.…”

An Experimental Model of Autoimmune Pancreatitis in the Rat

“…16 The pathogenicity of immunization with amylase was not tested in Uchida and colleague's 16 groundbreaking work so it is not known if amylase can be used to induce pancreatitis in immunologically crippled animals. It is known that thymectomy greatly increases the rate and sensitivity to autoantigens 17 and as a result, both our work and possibly the work of Uchida and colleagues 16 point to a T cell etiology of AIP. Thus it appears that in immunologically normal animals LF and CA-II are unable to induce EAP, whereas amylase can serve as a sufficient antigen.…”

Premature Ovarian Failure and Ovarian Autoimmunity

“…When CD4ϩCD8-thymocytes from normal neonatal or adult BALB/c mice are transferred to athymic mice, approximately 50 -75% of the recipients develop an autoimmune oö phoritis and/or gastritis (264). Neonatal CD4 ϩ splenocytes are also able to transfer the autoimmune diseases, whereas T cells from adult spleen do not (286). However, a fraction of adult spleen CD4 ϩ with a low expression of CD5 ϩ can induce oö phoritis in athymic recipients.…”