{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T04:09:51Z","timestamp":1790395791962,"version":"4.1.0"},"reference-count":59,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"5169","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[1994,7,8]]},"abstract":"<jats:p>\n            A switch from a T helper 1 (T\n            <jats:sub>H<\/jats:sub>\n            1) cytokine phenotype to a T\n            <jats:sub>H<\/jats:sub>\n            2 phenotype has been proposed as a critical element in the progression of human immunodeficiency virus (HIV) disease. Here, constitutive cytokine expression was analyzed in unfractionated and sorted cell populations isolated from peripheral blood and lymph nodes of HIV-infected individuals at different stages of disease. Expression of interleukin-2 (IL-2) and IL-4 was barely detectable (or undetectable) regardless of the stage of disease. CD8\n            <jats:sup>+<\/jats:sup>\n            cells expressed large amounts of interferon \u03b3 and IL-10, and the levels of these cytokines remained stably high throughout the course of infection. Furthermore, similar patterns of cytokine expression were observed after stimulation in vitro of purified CD4+ T cell populations obtained from HIV-infected individuals at different stages of disease. These results indicate that a switch from the T\n            <jats:sub>H<\/jats:sub>\n            1 to the T\n            <jats:sub>H<\/jats:sub>\n            2 cytokine phenotype does not occur during the progression of HIV disease.\n          <\/jats:p>","DOI":"10.1126\/science.8023143","type":"journal-article","created":{"date-parts":[[2006,10,6]],"date-time":"2006-10-06T00:01:25Z","timestamp":1160092885000},"page":"248-252","source":"Crossref","is-referenced-by-count":328,"title":["Lack of Evidence for the Dichotomy of T\n            <sub>H<\/sub>\n            1 and T\n            <sub>H<\/sub>\n            2 Predominance in HIV-Infected Individuals"],"prefix":"10.1126","volume":"265","author":[{"given":"Cecilia","family":"Graziosi","sequence":"first","affiliation":[{"name":"Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giuseppe","family":"Pantaleo","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kira R.","family":"Gantt","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Pierre","family":"Fortin","sequence":"additional","affiliation":[{"name":"Laboratory of Immunology, Institut de Recherches Cliniques de Montr\u00e9al, Montr\u00e9al, Qu\u00e9bec H2W 1 R7, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James F.","family":"Demarest","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oren J.","family":"Cohen","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rafick P.","family":"S\u00e9kaly","sequence":"additional","affiliation":[{"name":"Laboratory of Immunology, Institut de Recherches Cliniques de Montr\u00e9al, Montr\u00e9al, Qu\u00e9bec H2W 1 R7, Canada."},{"name":"D\u00e9partement de Microbiologie et d'lmmunologie, Universit\u00e9 de Montr\u00e9al, Montr\u00e9al, and Department of Microbiology and Immunology, McGill University, Montr\u00e9al, Qu\u00e9bec H3T 1 E2, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony S.","family":"Fauci","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"221","reference":[{"key":"e_1_2_1_1_1","doi-asserted-by":"crossref","first-page":"801","DOI":"10.7326\/0003-4819-100-6-801","volume":"100","year":"1984","unstructured":"ABRAMS, D.I., PERSISTENT DIFFUSE LYMPHADENOPATHY IN HOMOSEXUAL MEN - 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INDEPENDENCE OF CD4+ CELL NUMBERS AND CLINICAL STAGING, JOURNAL OF CLINICAL INVESTIGATION 84: 1892 (1989).","journal-title":"JOURNAL OF CLINICAL INVESTIGATION"},{"key":"e_1_2_1_9_1","doi-asserted-by":"crossref","first-page":"759","DOI":"10.1172\/JCI116294","volume":"91","year":"1993","unstructured":"CLERICI, M, CHANGES IN INTERLEUKIN-2 AND INTERLEUKIN-4 PRODUCTION IN ASYMPTOMATIC, HUMAN IMMUNODEFICIENCY VIRUS-SEROPOSITIVE INDIVIDUALS, JOURNAL OF CLINICAL INVESTIGATION 91: 759 (1993).","journal-title":"JOURNAL OF CLINICAL INVESTIGATION"},{"key":"e_1_2_1_10_1","doi-asserted-by":"crossref","first-page":"768","DOI":"10.1172\/JCI117031","volume":"93","year":"1994","unstructured":"CLERICI, M, ROLE OF INTERLEUKIN-10 IN T-HELPER CELL DYSFUNCTION IN ASYMPTOMATIC INDIVIDUALS INFECTED WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS, JOURNAL OF CLINICAL INVESTIGATION 93: 768 (1994).","journal-title":"JOURNAL OF CLINICAL INVESTIGATION"},{"key":"e_1_2_1_11_1","doi-asserted-by":"crossref","first-page":"961","DOI":"10.1056\/NEJM199104043241405","volume":"324","year":"1991","unstructured":"DAAR, E.S., TRANSIENT HIGH-LEVELS OF VIREMIA IN PATIENTS WITH PRIMARY HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION, NEW ENGLAND JOURNAL OF MEDICINE 324: 961 (1991).","journal-title":"NEW ENGLAND JOURNAL OF MEDICINE"},{"key":"e_1_2_1_12_1","doi-asserted-by":"crossref","first-page":"353","DOI":"10.4049\/jimmunol.150.2.353","volume":"150","year":"1993","unstructured":"DELPRETE, G, HUMAN IL-10 IS PRODUCED BY BOTH TYPE-1 HELPER (TH1) AND TYPE-2 HELPER (TH2) T-CELL CLONES AND INHIBITS THEIR ANTIGEN-SPECIFIC PROLIFERATION AND CYTOKINE PRODUCTION, JOURNAL OF IMMUNOLOGY 150: 353 (1993).","journal-title":"JOURNAL OF IMMUNOLOGY"},{"key":"e_1_2_1_13_1","doi-asserted-by":"crossref","first-page":"346","DOI":"10.1172\/JCI115300","volume":"88","year":"1991","unstructured":"DELPRETE, G.F., PURIFIED PROTEIN DERIVATIVE OF MYCOBACTERIUM-TUBERCULOSIS AND EXCRETORY-SECRETORY ANTIGEN(S) OF TOXOCARA-CANIS EXPAND INVITRO HUMAN T-CELLS WITH STABLE AND OPPOSITE (TYPE-1 T-HELPER OR TYPE-2 T-HELPER) PROFILE OF CYTOKINE PRODUCTION, JOURNAL OF CLINICAL INVESTIGATION 88: 346 (1991).","journal-title":"JOURNAL OF CLINICAL INVESTIGATION"},{"key":"e_1_2_1_14_1","doi-asserted-by":"crossref","first-page":"3133","DOI":"10.4049\/jimmunol.148.10.3133","volume":"148","year":"1992","unstructured":"DING, L, IL-10 INHIBITS MITOGEN-INDUCED T-CELL PROLIFERATION BY SELECTIVELY INHIBITING MACROPHAGE COSTIMULATORY FUNCTION, JOURNAL OF IMMUNOLOGY 148: 3133 (1992).","journal-title":"JOURNAL OF IMMUNOLOGY"},{"key":"e_1_2_1_15_1","doi-asserted-by":"crossref","first-page":"25","DOI":"10.1084\/jem.173.1.25","volume":"173","year":"1991","unstructured":"EHLERS, S, DIFFERENTIATION OF T-CELL LYMPHOKINE GENE-EXPRESSION - 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