Studies of HLA-B27-associated disease

Joel D Taurog; Jaime P. Durand; Fouad A K El-Zaatari; Robert E Hammer

doi:10.1016/0002-9343(88)90388-9

Studies of HLA-B27-associated disease

Joel D Taurog, Jaime P. Durand, Fouad A K El-Zaatari, Robert E Hammer

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3 Scopus citations

Abstract

Several rheumatic diseases were first shown to be associated with human leukocytic antigen (HLA)-B27 in 1973. Recent developments in understanding this association include the finding that there are at least six variants of HLA-B27 at the molecular level, with no one variant preferentially associated with disease. Detailed studies of the structure of the HLA-B27 molecular family are in progress in several laboratories. Mice expressing HLA-B27 and transmitting it to their offspring (transgenic mice) have been produced and are being studied for their response to bacteria that are known to trigger reactive arthritis in B27⁺ humans. A particular restriction fragment length polymorphism was recently claimed to be a genetic marker for an additional risk factor in ankylosing spondylitis, but two other laboratories have failed to confirm this finding.

Original language	English (US)
Pages (from-to)	59-60
Number of pages	2
Journal	The American Journal of Medicine
Volume	85
Issue number	6 SUPPL. 1
DOIs	https://doi.org/10.1016/0002-9343(88)90388-9
State	Published - Dec 23 1988

ASJC Scopus subject areas

Medicine(all)

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10.1016/0002-9343(88)90388-9

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title = "Studies of HLA-B27-associated disease",

abstract = "Several rheumatic diseases were first shown to be associated with human leukocytic antigen (HLA)-B27 in 1973. Recent developments in understanding this association include the finding that there are at least six variants of HLA-B27 at the molecular level, with no one variant preferentially associated with disease. Detailed studies of the structure of the HLA-B27 molecular family are in progress in several laboratories. Mice expressing HLA-B27 and transmitting it to their offspring (transgenic mice) have been produced and are being studied for their response to bacteria that are known to trigger reactive arthritis in B27+ humans. A particular restriction fragment length polymorphism was recently claimed to be a genetic marker for an additional risk factor in ankylosing spondylitis, but two other laboratories have failed to confirm this finding.",

author = "Taurog, {Joel D} and Durand, {Jaime P.} and El-Zaatari, {Fouad A K} and Hammer, {Robert E}",

note = "Funding Information: cine, and Howard Hughes Medical Instiie, University of Texas Southwestern Medical Center, flak, Texas. Thii study was supported by National lnstihutes of Health grant lnstiies of Health Research Career Development Award AR01756 (Dr. Taurog). Re quests for reorints should be addressed to Dr. Joel D. Taurog, Harold C. Simmons Arthritis Research Center, University of Texas Southwestern Medical Center, 5323 Hanv Hines Boulevard. Dallas. Texas 75235.",

year = "1988",

month = dec,

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doi = "10.1016/0002-9343(88)90388-9",

language = "English (US)",

volume = "85",

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T1 - Studies of HLA-B27-associated disease

AU - Taurog, Joel D

AU - Durand, Jaime P.

AU - El-Zaatari, Fouad A K

AU - Hammer, Robert E

N1 - Funding Information: cine, and Howard Hughes Medical Instiie, University of Texas Southwestern Medical Center, flak, Texas. Thii study was supported by National lnstihutes of Health grant lnstiies of Health Research Career Development Award AR01756 (Dr. Taurog). Re quests for reorints should be addressed to Dr. Joel D. Taurog, Harold C. Simmons Arthritis Research Center, University of Texas Southwestern Medical Center, 5323 Hanv Hines Boulevard. Dallas. Texas 75235.

PY - 1988/12/23

Y1 - 1988/12/23

N2 - Several rheumatic diseases were first shown to be associated with human leukocytic antigen (HLA)-B27 in 1973. Recent developments in understanding this association include the finding that there are at least six variants of HLA-B27 at the molecular level, with no one variant preferentially associated with disease. Detailed studies of the structure of the HLA-B27 molecular family are in progress in several laboratories. Mice expressing HLA-B27 and transmitting it to their offspring (transgenic mice) have been produced and are being studied for their response to bacteria that are known to trigger reactive arthritis in B27+ humans. A particular restriction fragment length polymorphism was recently claimed to be a genetic marker for an additional risk factor in ankylosing spondylitis, but two other laboratories have failed to confirm this finding.

AB - Several rheumatic diseases were first shown to be associated with human leukocytic antigen (HLA)-B27 in 1973. Recent developments in understanding this association include the finding that there are at least six variants of HLA-B27 at the molecular level, with no one variant preferentially associated with disease. Detailed studies of the structure of the HLA-B27 molecular family are in progress in several laboratories. Mice expressing HLA-B27 and transmitting it to their offspring (transgenic mice) have been produced and are being studied for their response to bacteria that are known to trigger reactive arthritis in B27+ humans. A particular restriction fragment length polymorphism was recently claimed to be a genetic marker for an additional risk factor in ankylosing spondylitis, but two other laboratories have failed to confirm this finding.

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JF - American Journal of Medicine

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Studies of HLA-B27-associated disease

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