Limited clonality in autoimmunity: Drivers and regulators

Peter Van Den Elzen, Juscilene S. Menezes, Akio Ametani, Emanual Michael Maverakis, Loui Madakamutil, Xiao Lei Tang, Vipin Kumar, Eli E. Sercarz

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The available T cell repertoire directed against self is appreciable owing to the escape of many clones from negative selection, largely because many determinants on self proteins are cryptic and not presented adequately. In addition, the degeneracy of T cell receptor specificity permits each lymphocyte a broad recognitive potential. Within the available self-reactive repertoire are T cells with high affinity, and these can compete favorably with other T cells with the same specificity. We have studied a "driver clone" and its two specific regulators in the B10.PL model of experimental autoimmune encephalomyelitis and found that each of these repertoires is highly limited. There is a single major clonal family comprising the aggressive driver population, which is public and of high affinity, and just one other minor public clonotype. The receptors of this Vβ8.2/Jβ2.7 driver are presented to a CD4 regulator and a CD8 suppressor, each of limited clonality, the latter killing the driver clone by apoptosis, completing a feedback control loop. This tightly regulated group of three cell types furnishes an excellent example of the immune homunculus.

Original languageEnglish (US)
Pages (from-to)524-529
Number of pages6
JournalAutoimmunity Reviews
Volume3
Issue number7-8 SPEC.ISS.
DOIs
StatePublished - Nov 2004
Externally publishedYes

Fingerprint

Autoimmunity
Clone Cells
T-Lymphocytes
T-Cell Antigen Receptor Specificity
Autoimmune Experimental Encephalomyelitis
Lymphocytes
Apoptosis
Population
Proteins

Keywords

  • Antigen processing
  • Competition
  • Degeneracy of T cell receptor recognition
  • Driver clones
  • Immune homunculus

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Van Den Elzen, P., Menezes, J. S., Ametani, A., Maverakis, E. M., Madakamutil, L., Tang, X. L., ... Sercarz, E. E. (2004). Limited clonality in autoimmunity: Drivers and regulators. Autoimmunity Reviews, 3(7-8 SPEC.ISS.), 524-529. https://doi.org/10.1016/j.autrev.2004.07.008

Limited clonality in autoimmunity : Drivers and regulators. / Van Den Elzen, Peter; Menezes, Juscilene S.; Ametani, Akio; Maverakis, Emanual Michael; Madakamutil, Loui; Tang, Xiao Lei; Kumar, Vipin; Sercarz, Eli E.

In: Autoimmunity Reviews, Vol. 3, No. 7-8 SPEC.ISS., 11.2004, p. 524-529.

Research output: Contribution to journalArticle

Van Den Elzen, P, Menezes, JS, Ametani, A, Maverakis, EM, Madakamutil, L, Tang, XL, Kumar, V & Sercarz, EE 2004, 'Limited clonality in autoimmunity: Drivers and regulators', Autoimmunity Reviews, vol. 3, no. 7-8 SPEC.ISS., pp. 524-529. https://doi.org/10.1016/j.autrev.2004.07.008
Van Den Elzen P, Menezes JS, Ametani A, Maverakis EM, Madakamutil L, Tang XL et al. Limited clonality in autoimmunity: Drivers and regulators. Autoimmunity Reviews. 2004 Nov;3(7-8 SPEC.ISS.):524-529. https://doi.org/10.1016/j.autrev.2004.07.008
Van Den Elzen, Peter ; Menezes, Juscilene S. ; Ametani, Akio ; Maverakis, Emanual Michael ; Madakamutil, Loui ; Tang, Xiao Lei ; Kumar, Vipin ; Sercarz, Eli E. / Limited clonality in autoimmunity : Drivers and regulators. In: Autoimmunity Reviews. 2004 ; Vol. 3, No. 7-8 SPEC.ISS. pp. 524-529.
@article{0872f5d4321a4c27b43020fff176ca98,
title = "Limited clonality in autoimmunity: Drivers and regulators",
abstract = "The available T cell repertoire directed against self is appreciable owing to the escape of many clones from negative selection, largely because many determinants on self proteins are cryptic and not presented adequately. In addition, the degeneracy of T cell receptor specificity permits each lymphocyte a broad recognitive potential. Within the available self-reactive repertoire are T cells with high affinity, and these can compete favorably with other T cells with the same specificity. We have studied a {"}driver clone{"} and its two specific regulators in the B10.PL model of experimental autoimmune encephalomyelitis and found that each of these repertoires is highly limited. There is a single major clonal family comprising the aggressive driver population, which is public and of high affinity, and just one other minor public clonotype. The receptors of this Vβ8.2/Jβ2.7 driver are presented to a CD4 regulator and a CD8 suppressor, each of limited clonality, the latter killing the driver clone by apoptosis, completing a feedback control loop. This tightly regulated group of three cell types furnishes an excellent example of the immune homunculus.",
keywords = "Antigen processing, Competition, Degeneracy of T cell receptor recognition, Driver clones, Immune homunculus",
author = "{Van Den Elzen}, Peter and Menezes, {Juscilene S.} and Akio Ametani and Maverakis, {Emanual Michael} and Loui Madakamutil and Tang, {Xiao Lei} and Vipin Kumar and Sercarz, {Eli E.}",
year = "2004",
month = "11",
doi = "10.1016/j.autrev.2004.07.008",
language = "English (US)",
volume = "3",
pages = "524--529",
journal = "Autoimmunity Reviews",
issn = "1568-9972",
publisher = "Elsevier",
number = "7-8 SPEC.ISS.",

}

TY - JOUR

T1 - Limited clonality in autoimmunity

T2 - Drivers and regulators

AU - Van Den Elzen, Peter

AU - Menezes, Juscilene S.

AU - Ametani, Akio

AU - Maverakis, Emanual Michael

AU - Madakamutil, Loui

AU - Tang, Xiao Lei

AU - Kumar, Vipin

AU - Sercarz, Eli E.

PY - 2004/11

Y1 - 2004/11

N2 - The available T cell repertoire directed against self is appreciable owing to the escape of many clones from negative selection, largely because many determinants on self proteins are cryptic and not presented adequately. In addition, the degeneracy of T cell receptor specificity permits each lymphocyte a broad recognitive potential. Within the available self-reactive repertoire are T cells with high affinity, and these can compete favorably with other T cells with the same specificity. We have studied a "driver clone" and its two specific regulators in the B10.PL model of experimental autoimmune encephalomyelitis and found that each of these repertoires is highly limited. There is a single major clonal family comprising the aggressive driver population, which is public and of high affinity, and just one other minor public clonotype. The receptors of this Vβ8.2/Jβ2.7 driver are presented to a CD4 regulator and a CD8 suppressor, each of limited clonality, the latter killing the driver clone by apoptosis, completing a feedback control loop. This tightly regulated group of three cell types furnishes an excellent example of the immune homunculus.

AB - The available T cell repertoire directed against self is appreciable owing to the escape of many clones from negative selection, largely because many determinants on self proteins are cryptic and not presented adequately. In addition, the degeneracy of T cell receptor specificity permits each lymphocyte a broad recognitive potential. Within the available self-reactive repertoire are T cells with high affinity, and these can compete favorably with other T cells with the same specificity. We have studied a "driver clone" and its two specific regulators in the B10.PL model of experimental autoimmune encephalomyelitis and found that each of these repertoires is highly limited. There is a single major clonal family comprising the aggressive driver population, which is public and of high affinity, and just one other minor public clonotype. The receptors of this Vβ8.2/Jβ2.7 driver are presented to a CD4 regulator and a CD8 suppressor, each of limited clonality, the latter killing the driver clone by apoptosis, completing a feedback control loop. This tightly regulated group of three cell types furnishes an excellent example of the immune homunculus.

KW - Antigen processing

KW - Competition

KW - Degeneracy of T cell receptor recognition

KW - Driver clones

KW - Immune homunculus

UR - http://www.scopus.com/inward/record.url?scp=8844233573&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=8844233573&partnerID=8YFLogxK

U2 - 10.1016/j.autrev.2004.07.008

DO - 10.1016/j.autrev.2004.07.008

M3 - Article

C2 - 15546801

AN - SCOPUS:8844233573

VL - 3

SP - 524

EP - 529

JO - Autoimmunity Reviews

JF - Autoimmunity Reviews

SN - 1568-9972

IS - 7-8 SPEC.ISS.

ER -