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Expression of murine IL-2 receptor beta-chain on thymic and splenic lymphocyte subpopulations as revealed by the IL-2-induced proliferative response in human IL-2 receptor alpha-chain transgenic mice.
J Immunol. 1990 May 15; 144(10):3809-15.JI

Abstract

Lymphocytes from the human (h) IL-2R alpha chain transgenic mice (TGM) constitutively express high affinity binding sites for hIL-2, consisting of transgenic h-IL-2R alpha and endogenous murine IL-2R beta, and therefore easily proliferate in vitro in response to hIL-2. Our study was undertaken to clarify the hIL-2-responsive lymphocyte subsets in the TGM, which should most likely reflect the normal distribution of m IL-2R beta expression. In both thymus and spleen, the majority of expanded cells by hIL-2 was CD3+CD4-CD8+ TCR alpha beta+ cells. The proliferation of CD4+ cells was not observed at all from either organ despite the expression of transgenic hIL-2R alpha. Potent cellular proliferation was also observed from the thymocytes that had been depleted of CD8+ cells, the expanded cells consisting of CD3- (15-40%) and CD3+ populations (60-85%). Among CD3+ cells, approximately the half portion expressed TCR alpha beta, whereas the other half was suggested to express TCR gamma delta. A variable portion (5-20%) of the CD3+ cells expressed CD8 (Lyt-2) in the absence of Lyt-3, and the CD3+CD8+ cells were confined preferentially to the TCR alpha beta- (TCR gamma delta+) population. In the culture of splenocytes depleted of CD8+ cells, however, the proliferated cells were mostly CD3-CD4-CD8-TCR-Mac1-, whereas a minor portion (10-30%) was CD3+CD4-CD8-TCR alpha beta- (TCR gamma delta+. Analysis of TCR genes at both DNA and mRNA levels confirmed the phenotypical observations. These results strongly suggested that IL-2R beta was constitutively and selectively expressed on the primary murine thymocytes and splenic T and NK cells, except for CD4+ cells in both organs.

Authors+Show Affiliations

Department of Veterinary Medicine, Hokkaido University, Sapporo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

2332632

Citation

Hattori, M, et al. "Expression of Murine IL-2 Receptor Beta-chain On Thymic and Splenic Lymphocyte Subpopulations as Revealed By the IL-2-induced Proliferative Response in Human IL-2 Receptor Alpha-chain Transgenic Mice." Journal of Immunology (Baltimore, Md. : 1950), vol. 144, no. 10, 1990, pp. 3809-15.
Hattori M, Okazaki H, Ishida Y, et al. Expression of murine IL-2 receptor beta-chain on thymic and splenic lymphocyte subpopulations as revealed by the IL-2-induced proliferative response in human IL-2 receptor alpha-chain transgenic mice. J Immunol. 1990;144(10):3809-15.
Hattori, M., Okazaki, H., Ishida, Y., Onuma, M., Kano, S., Honjo, T., & Minato, N. (1990). Expression of murine IL-2 receptor beta-chain on thymic and splenic lymphocyte subpopulations as revealed by the IL-2-induced proliferative response in human IL-2 receptor alpha-chain transgenic mice. Journal of Immunology (Baltimore, Md. : 1950), 144(10), 3809-15.
Hattori M, et al. Expression of Murine IL-2 Receptor Beta-chain On Thymic and Splenic Lymphocyte Subpopulations as Revealed By the IL-2-induced Proliferative Response in Human IL-2 Receptor Alpha-chain Transgenic Mice. J Immunol. 1990 May 15;144(10):3809-15. PubMed PMID: 2332632.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Expression of murine IL-2 receptor beta-chain on thymic and splenic lymphocyte subpopulations as revealed by the IL-2-induced proliferative response in human IL-2 receptor alpha-chain transgenic mice. AU - Hattori,M, AU - Okazaki,H, AU - Ishida,Y, AU - Onuma,M, AU - Kano,S, AU - Honjo,T, AU - Minato,N, PY - 1990/5/15/pubmed PY - 1990/5/15/medline PY - 1990/5/15/entrez SP - 3809 EP - 15 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 144 IS - 10 N2 - Lymphocytes from the human (h) IL-2R alpha chain transgenic mice (TGM) constitutively express high affinity binding sites for hIL-2, consisting of transgenic h-IL-2R alpha and endogenous murine IL-2R beta, and therefore easily proliferate in vitro in response to hIL-2. Our study was undertaken to clarify the hIL-2-responsive lymphocyte subsets in the TGM, which should most likely reflect the normal distribution of m IL-2R beta expression. In both thymus and spleen, the majority of expanded cells by hIL-2 was CD3+CD4-CD8+ TCR alpha beta+ cells. The proliferation of CD4+ cells was not observed at all from either organ despite the expression of transgenic hIL-2R alpha. Potent cellular proliferation was also observed from the thymocytes that had been depleted of CD8+ cells, the expanded cells consisting of CD3- (15-40%) and CD3+ populations (60-85%). Among CD3+ cells, approximately the half portion expressed TCR alpha beta, whereas the other half was suggested to express TCR gamma delta. A variable portion (5-20%) of the CD3+ cells expressed CD8 (Lyt-2) in the absence of Lyt-3, and the CD3+CD8+ cells were confined preferentially to the TCR alpha beta- (TCR gamma delta+) population. In the culture of splenocytes depleted of CD8+ cells, however, the proliferated cells were mostly CD3-CD4-CD8-TCR-Mac1-, whereas a minor portion (10-30%) was CD3+CD4-CD8-TCR alpha beta- (TCR gamma delta+. Analysis of TCR genes at both DNA and mRNA levels confirmed the phenotypical observations. These results strongly suggested that IL-2R beta was constitutively and selectively expressed on the primary murine thymocytes and splenic T and NK cells, except for CD4+ cells in both organs. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/2332632/Expression_of_murine_IL_2_receptor_beta_chain_on_thymic_and_splenic_lymphocyte_subpopulations_as_revealed_by_the_IL_2_induced_proliferative_response_in_human_IL_2_receptor_alpha_chain_transgenic_mice_ L2 - https://www.jimmunol.org/lookup/pmidlookup?view=long&pmid=2332632 DB - PRIME DP - Unbound Medicine ER -