Association of extensive polymorphisms in the SLAM/CD2 gene cluster with murine lupus

Amy E. Wandstrat; Charles Nguyen; Nisha Limaye; Alice Y. Chan; Srividya Subramanian; Xiang Hong Tian; Young Sun Yim; Alexander Pertsemlidis; Harold R. Garner; Laurence Morel; Edward K. Wakeland

doi:10.1016/j.immuni.2004.10.009

Association of extensive polymorphisms in the SLAM/CD2 gene cluster with murine lupus

Amy E. Wandstrat
, Charles Nguyen
, Nisha Limaye
, Alice Y. Chan
, Srividya Subramanian
, Xiang Hong Tian
, Young Sun Yim
, Alexander Pertsemlidis
, Harold R. Garner
, Laurence Morel
, Edward K. Wakeland

Research output: Contribution to journal › Article › peer-review

242 Scopus citations

Abstract

Susceptibility to autoimmunity in B6.Sle1b mice is associated with extensive polymorphisms between two divergent haplotypes of the SLAM/CD2 family of genes. The B6.Sle1b-derived SLAM/CD2 family haplotype is found in many other laboratory mouse strains but only causes autoimmunity in the context of the C57Bl/6 (B6) genome. Phenotypic analyses have revealed variations in the structure and expression of several members of the SLAM/CD2 family in T and B lymphocytes from B6.Sle1b mice. T lymphocytes from B6.Sle1b mice have modified signaling responses to stimulation at 4-6 weeks of age. While autoimmunity may be mediated by a combination of genes in the SLAM/CD2 family cluster, the strongest candidate is Ly108, a specific isoform of which is constitutively upregulated in B6.Sle1b lymphocytes.

Original language	English (US)
Pages (from-to)	769-780
Number of pages	12
Journal	Immunity
Volume	21
Issue number	6
DOIs	https://doi.org/10.1016/j.immuni.2004.10.009
State	Published - Dec 2004
Externally published	Yes

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Infectious Diseases

Access to Document

10.1016/j.immuni.2004.10.009

Cite this

@article{f754d0b4a5264ac8ba93664d581ea76c,

title = "Association of extensive polymorphisms in the SLAM/CD2 gene cluster with murine lupus",

abstract = "Susceptibility to autoimmunity in B6.Sle1b mice is associated with extensive polymorphisms between two divergent haplotypes of the SLAM/CD2 family of genes. The B6.Sle1b-derived SLAM/CD2 family haplotype is found in many other laboratory mouse strains but only causes autoimmunity in the context of the C57Bl/6 (B6) genome. Phenotypic analyses have revealed variations in the structure and expression of several members of the SLAM/CD2 family in T and B lymphocytes from B6.Sle1b mice. T lymphocytes from B6.Sle1b mice have modified signaling responses to stimulation at 4-6 weeks of age. While autoimmunity may be mediated by a combination of genes in the SLAM/CD2 family cluster, the strongest candidate is Ly108, a specific isoform of which is constitutively upregulated in B6.Sle1b lymphocytes.",

author = "Wandstrat, \{Amy E.\} and Charles Nguyen and Nisha Limaye and Chan, \{Alice Y.\} and Srividya Subramanian and Tian, \{Xiang Hong\} and Yim, \{Young Sun\} and Alexander Pertsemlidis and Garner, \{Harold R.\} and Laurence Morel and Wakeland, \{Edward K.\}",

note = "Funding Information: We thank Dr. Jose Casco for the maintenance of mice. David Chambliss provided excellent technical assistance in these studies. This work was supported by grants from the National Institutes of Health (NIH), The Alliance for Lupus Research, The Lupus Research Institute, and the Arthritis Foundation (E.K.W.). A.E.W. was supported by an NIH postdoctoral fellowship and by a grant from the Lupus Foundation. N.L. was supported in part by a grant from the National Institute of Allergy and Infectious Disease, T32AI005284. ",

year = "2004",

month = dec,

doi = "10.1016/j.immuni.2004.10.009",

language = "English (US)",

volume = "21",

pages = "769--780",

journal = "Immunity",

issn = "1074-7613",

publisher = "Cell Press",

number = "6",

}

TY - JOUR

T1 - Association of extensive polymorphisms in the SLAM/CD2 gene cluster with murine lupus

AU - Wandstrat, Amy E.

AU - Nguyen, Charles

AU - Limaye, Nisha

AU - Chan, Alice Y.

AU - Subramanian, Srividya

AU - Tian, Xiang Hong

AU - Yim, Young Sun

AU - Pertsemlidis, Alexander

AU - Garner, Harold R.

AU - Morel, Laurence

AU - Wakeland, Edward K.

N1 - Funding Information: We thank Dr. Jose Casco for the maintenance of mice. David Chambliss provided excellent technical assistance in these studies. This work was supported by grants from the National Institutes of Health (NIH), The Alliance for Lupus Research, The Lupus Research Institute, and the Arthritis Foundation (E.K.W.). A.E.W. was supported by an NIH postdoctoral fellowship and by a grant from the Lupus Foundation. N.L. was supported in part by a grant from the National Institute of Allergy and Infectious Disease, T32AI005284.

PY - 2004/12

Y1 - 2004/12

N2 - Susceptibility to autoimmunity in B6.Sle1b mice is associated with extensive polymorphisms between two divergent haplotypes of the SLAM/CD2 family of genes. The B6.Sle1b-derived SLAM/CD2 family haplotype is found in many other laboratory mouse strains but only causes autoimmunity in the context of the C57Bl/6 (B6) genome. Phenotypic analyses have revealed variations in the structure and expression of several members of the SLAM/CD2 family in T and B lymphocytes from B6.Sle1b mice. T lymphocytes from B6.Sle1b mice have modified signaling responses to stimulation at 4-6 weeks of age. While autoimmunity may be mediated by a combination of genes in the SLAM/CD2 family cluster, the strongest candidate is Ly108, a specific isoform of which is constitutively upregulated in B6.Sle1b lymphocytes.

AB - Susceptibility to autoimmunity in B6.Sle1b mice is associated with extensive polymorphisms between two divergent haplotypes of the SLAM/CD2 family of genes. The B6.Sle1b-derived SLAM/CD2 family haplotype is found in many other laboratory mouse strains but only causes autoimmunity in the context of the C57Bl/6 (B6) genome. Phenotypic analyses have revealed variations in the structure and expression of several members of the SLAM/CD2 family in T and B lymphocytes from B6.Sle1b mice. T lymphocytes from B6.Sle1b mice have modified signaling responses to stimulation at 4-6 weeks of age. While autoimmunity may be mediated by a combination of genes in the SLAM/CD2 family cluster, the strongest candidate is Ly108, a specific isoform of which is constitutively upregulated in B6.Sle1b lymphocytes.

UR - https://www.scopus.com/pages/publications/10344252778

UR - https://www.scopus.com/pages/publications/10344252778#tab=citedBy

U2 - 10.1016/j.immuni.2004.10.009

DO - 10.1016/j.immuni.2004.10.009

M3 - Article

C2 - 15589166

AN - SCOPUS:10344252778

SN - 1074-7613

VL - 21

SP - 769

EP - 780

JO - Immunity

JF - Immunity

IS - 6

ER -

Association of extensive polymorphisms in the SLAM/CD2 gene cluster with murine lupus

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this