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Correction of T Cell Function by Thymosin in New Zealand Mice¹

From the Arthritis and Rheumatism Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, Maryland 20014, the Experimental Immunology Division, Naval Medical Research Institute, Bethesda, Maryland 20014, and the Department of Biochemistry, University of Texas, Galveston, Texas 77550

Abstract

There has been a great deal of interest in the preparation and purification of thymosin, a soluble product of calf thymus (1). This material is believed to be a thymic hormone and like other similar thymic factors described (2) is capable of restoring skin allograft rejection and ability to induce graft-vs-host (GVH)⁵ disease in neonatally thymectomized mice (3, 4). Further thymosin stimulates lymphoid tissue growth (4), and induces the appearance of T cell markers in bone marrow cells (5). There have been many suggestions that thymosin is critical in preventing autoimmune disease in humans. Indeed levels of thymic hormones are reported low in systemic lupus erythematosus (SLE), and are stated to decrease with age (6).

New Zealand NZB x NZW F₁ (NZB/W) female mice, after 7 months of age, manifest a large number of immunologic abnormalities including decreased ability to reject skin allografts, decline in capacity of lymphoid cells to respond to allogeneic cells or other mitogens, and diminished primary response to sheep red blood cells (SRBC).

Footnotes

¹ These studies were supported by Grants CA 14108 and CA 15419 from the National Cancer Institute and by the John A. Hartford Foundation, Inc.

⁵ Abbreviations used in this paper: GVH, graft-vs-host; SLE; systemic lupus erythematosus; SRBC, sheep red blood cells; NTA, natural thymocytotoxic antibody; BSA, bovine serum albumin; PHA-P, phytohemagglutinin A; LPS, Escherichia coli lipopolysaccharide; Con A, concanavalin A; ³H-TdR, ³H-thymidine; MLR, mixed lymphocyte reaction; polyI-polyC, polyriboinosinic polyribocytidylic acid.

² Arthritis and Rheumatism Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, Maryland 20014.

³ Experimental Immunology Division, The Naval Medical Research Institute, Bethesda, Maryland 20014.

⁴ Department of Biochemistry, University of Texas, Galveston, Texas 77550.

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