Polymyositis mediated by T lymphocytes that express the γ/δ receptor

R. Hohlfeld, Andrew G Engel, K. Ii, M. C. Harper

Research output: Contribution to journalArticle

128 Citations (Scopus)

Abstract

Background. The invasion and destruction of nonnecrotic muscle fibers by CD8± cytotoxic T cells is considered a hallmark of polymyositis. In the cases of polymyositis reported so far, the autoinvasive CD8+ T cells expressed the common form of T-cell receptor for the recognition of antigen, the so-called α/β T-cell receptor. We describe a 69-year-old man with polymyositis mediated by CD4-, CD8- T cells expressing the recently discovered, uncommon γδ T-cell receptor. Methods. We used immunofluorescence or immunoperoxidase techniques to study frozen sections of muscle from our patient, who had mild weakness of cervical and proximal limb muscles, and from control patients with polymyositis, inclusion-body myositis, dermatomyositis, or granulomatous myopathy with monoclonal antibodies against T-cell-related antigens (CD2, CD3, CD4, CD8, and γβ T-cell receptor), B cells (CD22), major histocompatibility complex (MHC) and MHC-related antigens (MHC Class I, CD1a, CD1b, and CD1c), and the 65-kd heatshock protein. The membrane contacts between the autoinvasive cells and the sarcolemma were investigated by electron microscopy. Results. In the patient described here, but not in 28 others with inflammatory myopathies, myriad γδ T cells surrounded and invaded nonnecrotic muscle fibers. All muscle fibers were highly reactive for MHC Class I antigen and the 65-kd heat-shock protein. Treatment with prednisone improved the clinical and histologic findings. Conclusions. Polymyositis can be mediated by γδ T cells. This new form of polymyositis appears to be highly responsive to steroids.

Original languageEnglish (US)
Pages (from-to)877-881
Number of pages5
JournalNew England Journal of Medicine
Volume324
Issue number13
StatePublished - 1991

Fingerprint

Polymyositis
T-Cell Antigen Receptor
Major Histocompatibility Complex
T-Lymphocytes
Muscles
CD2 Antigens
Inclusion Body Myositis
CD3 Antigens
Sarcolemma
Histocompatibility Antigens Class I
Myositis
Dermatomyositis
Frozen Sections
Muscular Diseases
Heat-Shock Proteins
Prednisone
Immunoenzyme Techniques
Fluorescent Antibody Technique
Electron Microscopy
B-Lymphocytes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Polymyositis mediated by T lymphocytes that express the γ/δ receptor. / Hohlfeld, R.; Engel, Andrew G; Ii, K.; Harper, M. C.

In: New England Journal of Medicine, Vol. 324, No. 13, 1991, p. 877-881.

Research output: Contribution to journalArticle

Hohlfeld, R. ; Engel, Andrew G ; Ii, K. ; Harper, M. C. / Polymyositis mediated by T lymphocytes that express the γ/δ receptor. In: New England Journal of Medicine. 1991 ; Vol. 324, No. 13. pp. 877-881.
@article{c24fb13381574993b75a3f5104d7d732,
title = "Polymyositis mediated by T lymphocytes that express the γ/δ receptor",
abstract = "Background. The invasion and destruction of nonnecrotic muscle fibers by CD8± cytotoxic T cells is considered a hallmark of polymyositis. In the cases of polymyositis reported so far, the autoinvasive CD8+ T cells expressed the common form of T-cell receptor for the recognition of antigen, the so-called α/β T-cell receptor. We describe a 69-year-old man with polymyositis mediated by CD4-, CD8- T cells expressing the recently discovered, uncommon γδ T-cell receptor. Methods. We used immunofluorescence or immunoperoxidase techniques to study frozen sections of muscle from our patient, who had mild weakness of cervical and proximal limb muscles, and from control patients with polymyositis, inclusion-body myositis, dermatomyositis, or granulomatous myopathy with monoclonal antibodies against T-cell-related antigens (CD2, CD3, CD4, CD8, and γβ T-cell receptor), B cells (CD22), major histocompatibility complex (MHC) and MHC-related antigens (MHC Class I, CD1a, CD1b, and CD1c), and the 65-kd heatshock protein. The membrane contacts between the autoinvasive cells and the sarcolemma were investigated by electron microscopy. Results. In the patient described here, but not in 28 others with inflammatory myopathies, myriad γδ T cells surrounded and invaded nonnecrotic muscle fibers. All muscle fibers were highly reactive for MHC Class I antigen and the 65-kd heat-shock protein. Treatment with prednisone improved the clinical and histologic findings. Conclusions. Polymyositis can be mediated by γδ T cells. This new form of polymyositis appears to be highly responsive to steroids.",
author = "R. Hohlfeld and Engel, {Andrew G} and K. Ii and Harper, {M. C.}",
year = "1991",
language = "English (US)",
volume = "324",
pages = "877--881",
journal = "New England Journal of Medicine",
issn = "1533-4406",
publisher = "Massachussetts Medical Society",
number = "13",

}

TY - JOUR

T1 - Polymyositis mediated by T lymphocytes that express the γ/δ receptor

AU - Hohlfeld, R.

AU - Engel, Andrew G

AU - Ii, K.

AU - Harper, M. C.

PY - 1991

Y1 - 1991

N2 - Background. The invasion and destruction of nonnecrotic muscle fibers by CD8± cytotoxic T cells is considered a hallmark of polymyositis. In the cases of polymyositis reported so far, the autoinvasive CD8+ T cells expressed the common form of T-cell receptor for the recognition of antigen, the so-called α/β T-cell receptor. We describe a 69-year-old man with polymyositis mediated by CD4-, CD8- T cells expressing the recently discovered, uncommon γδ T-cell receptor. Methods. We used immunofluorescence or immunoperoxidase techniques to study frozen sections of muscle from our patient, who had mild weakness of cervical and proximal limb muscles, and from control patients with polymyositis, inclusion-body myositis, dermatomyositis, or granulomatous myopathy with monoclonal antibodies against T-cell-related antigens (CD2, CD3, CD4, CD8, and γβ T-cell receptor), B cells (CD22), major histocompatibility complex (MHC) and MHC-related antigens (MHC Class I, CD1a, CD1b, and CD1c), and the 65-kd heatshock protein. The membrane contacts between the autoinvasive cells and the sarcolemma were investigated by electron microscopy. Results. In the patient described here, but not in 28 others with inflammatory myopathies, myriad γδ T cells surrounded and invaded nonnecrotic muscle fibers. All muscle fibers were highly reactive for MHC Class I antigen and the 65-kd heat-shock protein. Treatment with prednisone improved the clinical and histologic findings. Conclusions. Polymyositis can be mediated by γδ T cells. This new form of polymyositis appears to be highly responsive to steroids.

AB - Background. The invasion and destruction of nonnecrotic muscle fibers by CD8± cytotoxic T cells is considered a hallmark of polymyositis. In the cases of polymyositis reported so far, the autoinvasive CD8+ T cells expressed the common form of T-cell receptor for the recognition of antigen, the so-called α/β T-cell receptor. We describe a 69-year-old man with polymyositis mediated by CD4-, CD8- T cells expressing the recently discovered, uncommon γδ T-cell receptor. Methods. We used immunofluorescence or immunoperoxidase techniques to study frozen sections of muscle from our patient, who had mild weakness of cervical and proximal limb muscles, and from control patients with polymyositis, inclusion-body myositis, dermatomyositis, or granulomatous myopathy with monoclonal antibodies against T-cell-related antigens (CD2, CD3, CD4, CD8, and γβ T-cell receptor), B cells (CD22), major histocompatibility complex (MHC) and MHC-related antigens (MHC Class I, CD1a, CD1b, and CD1c), and the 65-kd heatshock protein. The membrane contacts between the autoinvasive cells and the sarcolemma were investigated by electron microscopy. Results. In the patient described here, but not in 28 others with inflammatory myopathies, myriad γδ T cells surrounded and invaded nonnecrotic muscle fibers. All muscle fibers were highly reactive for MHC Class I antigen and the 65-kd heat-shock protein. Treatment with prednisone improved the clinical and histologic findings. Conclusions. Polymyositis can be mediated by γδ T cells. This new form of polymyositis appears to be highly responsive to steroids.

UR - http://www.scopus.com/inward/record.url?scp=0025752993&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025752993&partnerID=8YFLogxK

M3 - Article

C2 - 1705662

AN - SCOPUS:0025752993

VL - 324

SP - 877

EP - 881

JO - New England Journal of Medicine

JF - New England Journal of Medicine

SN - 1533-4406

IS - 13

ER -