Development of CD8{alpha}/{alpha} and CD8{alpha}/{beta} T Cells in Major Histocompatibility Complex Class I–deficient Mice

doi:10.1084/jem.190.6.881

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© The Rockefeller University Press, 0022-1007/1999/9/881/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 6, September 20, 1999 881-884

Development of CD8 ${alpha}$ / ${alpha}$ and CD8 ${alpha}$ /ß T Cells in Major Histocompatibility Complex Class I–deficient Mice

Gobardhan Das^a and Charles A. Janeway, Jr.^a
^a Howard Hughes Medical Institute and Yale University Medical School, New Haven, Connecticut 06510

Correspondence to: Charles A. Janeway, Jr., LH-416, Howard Hughes Medical Institute and Yale University School of Medicine, 310 Cedar St., New Haven, CT 06510. Tel:203-785-2793 Fax:203-737-1765 E-mail:charles.janeway{at}yale.edu.

Peripheral CD8⁺ T cells mainly use CD8 ${alpha}$ /ß, and their developmentis mainly dependent on the major histocompatibility complex(MHC) class I proteins K^b and D^b in H-2^b mice. In this report,we have shown that the development of CD8 ${alpha}$ /ß TCR- ${alpha}$ /ßcells in lymphoid organs as well as in intestinal intraepitheliallymphocytes (iIELs) is dependent on the MHC class I K^b and D^bproteins. In contrast, TCR- ${alpha}$ /ß CD8 ${alpha}$ / ${alpha}$ cells are found mainlyin iIELs, and their numbers are unaffected in K^bD^b double knockoutmice. Most of the TCR- ${gamma}$ / ${delta}$ cells in the iIELs also bear CD8 ${alpha}$ / ${alpha}$ , andthey are also unaffected in K^bD^b -/- mice. In ß2-microglobulin(ß2m)-deficient mice, all of the TCR- ${alpha}$ /ß CD8 ${alpha}$ / ${alpha}$ andCD8 ${alpha}$ /ß T cells disappear, but TCR- ${gamma}$ / ${delta}$ cells are unaffectedby the absence of ß2m.

Key Words: CD8 ${alpha}$ / ${alpha}$ T cells, CD8 ${alpha}$ /ß T cells, major histocompatibilitycomplex class I, K^bD^b-deficient mice, ß2m-deficient mice

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Development of CD8/ and CD8/ß T Cells in Major Histocompatibility Complex Class I–deficient Mice

Development of CD8 ${alpha}$ / ${alpha}$ and CD8 ${alpha}$ /ß T Cells in Major Histocompatibility Complex Class I–deficient Mice