{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T19:15:19Z","timestamp":1781118919233,"version":"3.54.1"},"reference-count":47,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2005,11,17]],"date-time":"2005-11-17T00:00:00Z","timestamp":1132185600000},"content-version":"vor","delay-in-days":3822,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1995,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Certain infections, like that with the human immunodeficiency virus\u20101, deplete vitamin A, and when vitamin A levels are low, immune dysfunctions establish susceptibility to further infection. Our research has focused on the immune dysfunctions that are a consequence of vitamin A deficiency and that predispose to further infection. We previously studied a helminth infection in mice, and showed that when vitamin A levels are low, the immune response develops a strong regulatory T cell imbalance with excessive T helper type\u20101 cell interferon (IFN)\u2010\u03b3 synthesis and insufficient T helper type\u20102 cell development and function. Here, we studied the T cell priming environment in vitamin A\u2010deficient mice to learn how that priming environment might produce a regulatory T cell imbalance and consequently distort the ability of the immune system to respond to an infection. Our results show that during vitamin A deficiency, the priming environment included constitutive interleukin (IL)\u201012 and IFN\u2010\u03b3 transcripts, but it was devoid of constitutive IL\u20104 and IL\u201010 transcripts. Dietary all\u2010<jats:italic>trans<\/jats:italic>\u2010retinoic acid supplementation down\u2010regulated the level of constitutive IL\u201012 and IFN\u2010\u03b3 transcripts. Furthermore, when T cells from naive vitamin A\u2010deficient animals were stimulated through the T cell receptor, they produced excess IFN\u2010\u03b3 protein compared to T cells from control animals. In contrast, T cell stimulation failed to induce IL\u20104 or IL\u201010 secretion. The inducible IFN\u2010\u03b3 was largely from CD8<jats:sup>+<\/jats:sup> T cells and all\u2010<jats:italic>trans<\/jats:italic>\u2010retinoic acid addition <jats:italic>in vitro<\/jats:italic> inhibited IFN\u2010\u03b3 production at the transcript level. Retinoic acid addition <jats:italic>in vitro<\/jats:italic> also decreased natural killer cell IFN\u2010\u03b3 synthesis at the transcript level. Taken together, the distorted constitutive and inducible cytokine gene expression patterns that occurred when vitamin A levels were low would be expected strongly to favor T helper type\u20101 development and limit T helper type\u20102 cell growth and differentiation, thereby limiting the animal's humoral immune response capability.<\/jats:p>","DOI":"10.1002\/eji.1830250629","type":"journal-article","created":{"date-parts":[[2007,3,2]],"date-time":"2007-03-02T00:48:40Z","timestamp":1172796520000},"page":"1673-1679","source":"Crossref","is-referenced-by-count":104,"title":["Vitamin A deficiency results in a priming environment conducive for Th1 cell development"],"prefix":"10.1002","volume":"25","author":[{"given":"Margherita T.","family":"Cantorna","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Faye E.","family":"Nashold","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Colleen E.","family":"Hayes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,11,17]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"crossref","first-page":"2149","DOI":"10.1001\/archinte.1993.00410180103012","volume":"153","author":"Semba R. 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