TCRBV CDR3 diversity of CD4+ and CD8+ T-lymphocytes in HIV-infected individuals

Frank M. Raaphorst; Robert L. Schelonka; Janice Rusnak; Anthony J. Infante; Judy M. Teale

doi:10.1016/S0198-8859(01)00361-5

TCRBV CDR3 diversity of CD4+ and CD8+ T-lymphocytes in HIV-infected individuals

Frank M. Raaphorst
, Robert L. Schelonka
, Janice Rusnak
, Anthony J. Infante
, Judy M. Teale

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

16 Scopus citations

Abstract

TCRBV CDR3 repertoire diversity was analyzed in a cross-sectional study of HIV-infected individuals by CDR3 fingerprinting/spectratyping and single strand conformation polymorphism (SSCP). Most TCRBV families were detected in CD4⁺ cells of HIV-infected patients with CD4 counts ranging from 35 to 1103. In patients with CD4 counts >500, CD4⁺ TCRBV CDR3 fingerprinting profiles contained subtle variations with generally gaussian-distributed sizes. Lower CD4 counts coincided with more fragmented TCRBV CDR3 repertoires, containg dominant bands and bands missing from the CDR3 profiles. The CD8⁺ population of the same patients exhibited skewed CDR3 profiles of the majority of TCR BV families at CD4 counts >500. Irregularity of CD8⁺ CDR3 size distribution was most profound at low CD4 counts and suggested domination of the CD8⁺ TCRBV repertoire by a limited number of clones. Skewed patterns of CDR3 diversity probably reflect (oligo)clonal expansion of particular CD4⁺ and CD8⁺ cell populations during chronic infection with HIV. In addition, irregular CDR3 profiles of CD4⁺ and CD8⁺ at low CD4 counts suggest diminished TCR repertoire diversity, which may contribute to immunodeficiency.

Original language	English (US)
Pages (from-to)	51-60
Number of pages	10
Journal	Human Immunology
Volume	63
Issue number	1
DOIs	https://doi.org/10.1016/S0198-8859(01)00361-5
State	Published - 2002
Externally published	Yes

Funding

We thank Dr. Frank Miedema of the Dutch Red Cross Bloodtransfusion Service in Amsterdam (Department of Clinical Immunovirology) for his critical comments and valuable suggestions. These studies were supported by the Surgeon General’s office (Grant #96-046 to R.L.S.), the National Institutes of Health (Grants AI 19896, AI 33221 and NS 35974 to J.M.T. and Grant AI 33195 to A.J.I.), the Henry M. Jackson Foundation, and the Military Medical Consortium for Applied Retroviral Research (MMCARR). The views expressed in this article are those of the authors and do not reflect the official policy of the Department of Defense or other Departments of the U.S. Government.

Funders	Funder number
Military Medical Consortium for Applied Retroviral Research
HQ USAF Surgeon General’s Office	96-046
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health	AI 33195, NS 35974, AI 33221
National Institute of Allergy and Infectious Diseases	R37AI019896
Henry M. Jackson Foundation

Keywords

CDR3 spectratyping
HIV infection
T-cell receptor repertoire

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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10.1016/S0198-8859(01)00361-5

Cite this

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title = "TCRBV CDR3 diversity of CD4+ and CD8+ T-lymphocytes in HIV-infected individuals",

abstract = "TCRBV CDR3 repertoire diversity was analyzed in a cross-sectional study of HIV-infected individuals by CDR3 fingerprinting/spectratyping and single strand conformation polymorphism (SSCP). Most TCRBV families were detected in CD4+ cells of HIV-infected patients with CD4 counts ranging from 35 to 1103. In patients with CD4 counts >500, CD4+ TCRBV CDR3 fingerprinting profiles contained subtle variations with generally gaussian-distributed sizes. Lower CD4 counts coincided with more fragmented TCRBV CDR3 repertoires, containg dominant bands and bands missing from the CDR3 profiles. The CD8+ population of the same patients exhibited skewed CDR3 profiles of the majority of TCR BV families at CD4 counts >500. Irregularity of CD8+ CDR3 size distribution was most profound at low CD4 counts and suggested domination of the CD8+ TCRBV repertoire by a limited number of clones. Skewed patterns of CDR3 diversity probably reflect (oligo)clonal expansion of particular CD4+ and CD8+ cell populations during chronic infection with HIV. In addition, irregular CDR3 profiles of CD4+ and CD8+ at low CD4 counts suggest diminished TCR repertoire diversity, which may contribute to immunodeficiency.",

keywords = "CDR3 spectratyping, HIV infection, T-cell receptor repertoire",

author = "Raaphorst, \{Frank M.\} and Schelonka, \{Robert L.\} and Janice Rusnak and Infante, \{Anthony J.\} and Teale, \{Judy M.\}",

note = "Funding Information: We thank Dr. Frank Miedema of the Dutch Red Cross Bloodtransfusion Service in Amsterdam (Department of Clinical Immunovirology) for his critical comments and valuable suggestions. These studies were supported by the Surgeon General{\textquoteright}s office (Grant \#96-046 to R.L.S.), the National Institutes of Health (Grants AI 19896, AI 33221 and NS 35974 to J.M.T. and Grant AI 33195 to A.J.I.), the Henry M. Jackson Foundation, and the Military Medical Consortium for Applied Retroviral Research (MMCARR). The views expressed in this article are those of the authors and do not reflect the official policy of the Department of Defense or other Departments of the U.S. Government.",

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doi = "10.1016/S0198-8859(01)00361-5",

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AU - Infante, Anthony J.

AU - Teale, Judy M.

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N2 - TCRBV CDR3 repertoire diversity was analyzed in a cross-sectional study of HIV-infected individuals by CDR3 fingerprinting/spectratyping and single strand conformation polymorphism (SSCP). Most TCRBV families were detected in CD4+ cells of HIV-infected patients with CD4 counts ranging from 35 to 1103. In patients with CD4 counts >500, CD4+ TCRBV CDR3 fingerprinting profiles contained subtle variations with generally gaussian-distributed sizes. Lower CD4 counts coincided with more fragmented TCRBV CDR3 repertoires, containg dominant bands and bands missing from the CDR3 profiles. The CD8+ population of the same patients exhibited skewed CDR3 profiles of the majority of TCR BV families at CD4 counts >500. Irregularity of CD8+ CDR3 size distribution was most profound at low CD4 counts and suggested domination of the CD8+ TCRBV repertoire by a limited number of clones. Skewed patterns of CDR3 diversity probably reflect (oligo)clonal expansion of particular CD4+ and CD8+ cell populations during chronic infection with HIV. In addition, irregular CDR3 profiles of CD4+ and CD8+ at low CD4 counts suggest diminished TCR repertoire diversity, which may contribute to immunodeficiency.

AB - TCRBV CDR3 repertoire diversity was analyzed in a cross-sectional study of HIV-infected individuals by CDR3 fingerprinting/spectratyping and single strand conformation polymorphism (SSCP). Most TCRBV families were detected in CD4+ cells of HIV-infected patients with CD4 counts ranging from 35 to 1103. In patients with CD4 counts >500, CD4+ TCRBV CDR3 fingerprinting profiles contained subtle variations with generally gaussian-distributed sizes. Lower CD4 counts coincided with more fragmented TCRBV CDR3 repertoires, containg dominant bands and bands missing from the CDR3 profiles. The CD8+ population of the same patients exhibited skewed CDR3 profiles of the majority of TCR BV families at CD4 counts >500. Irregularity of CD8+ CDR3 size distribution was most profound at low CD4 counts and suggested domination of the CD8+ TCRBV repertoire by a limited number of clones. Skewed patterns of CDR3 diversity probably reflect (oligo)clonal expansion of particular CD4+ and CD8+ cell populations during chronic infection with HIV. In addition, irregular CDR3 profiles of CD4+ and CD8+ at low CD4 counts suggest diminished TCR repertoire diversity, which may contribute to immunodeficiency.

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TCRBV CDR3 diversity of CD4+ and CD8+ T-lymphocytes in HIV-infected individuals

Abstract

Funding

Keywords

ASJC Scopus subject areas

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