Koch's postulates and autoimmunity: An opposing viewpoint

Chaim Putterman, Yaakov Naparstek

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Autoimmunity is characterized as a state of abnormal specific humoral and cell-mediated responses against constituents of body tissues. One time- honored approach to explaining the pathogenesis of autoimmunity has been application of the Koch's postulates, on loan from the field of microbiology suggesting that autoantibodies and/or autoreactive T cells are the presumed 'pathogens' of autoimmunity, and that passive transfer of these autoimmune factors to susceptible animals will result in the induction of the autoimmune disease. We suggest that autoimmunity is not in many cases due to the presence of factors leading to the autoimmune response in those susceptible. Instead, it is the lack of a factor which leads to the development of autoimmunity, a factor (cytokine, protein, gene, etc.) which is present in the healthy individual and normally protects in from disordered immune regulation. We propose to direct more research into therapeutic modulation of autoimmunity by administration of putative 'protective factors', rather than by attempts to depress or remove autoreactive cells and antibodies from the autoimmune.

Original languageEnglish (US)
Pages (from-to)25-32
Number of pages8
JournalArchivum Immunologiae et Therapiae Experimentalis
Volume47
Issue number1
StatePublished - 1999
Externally publishedYes

Fingerprint

Autoimmunity
Therapeutic Human Experimentation
Transfer Factor
Microbiology
Autoantibodies
Autoimmune Diseases
Cytokines
T-Lymphocytes
Antibodies
Proteins

Keywords

  • Autoantibodies
  • Autoimmunity
  • Autoreactive cells
  • Pathogenesis

ASJC Scopus subject areas

  • Immunology

Cite this

Koch's postulates and autoimmunity : An opposing viewpoint. / Putterman, Chaim; Naparstek, Yaakov.

In: Archivum Immunologiae et Therapiae Experimentalis, Vol. 47, No. 1, 1999, p. 25-32.

Research output: Contribution to journalArticle

@article{2955f724f9bd4a99ba1940acbee3e3dc,
title = "Koch's postulates and autoimmunity: An opposing viewpoint",
abstract = "Autoimmunity is characterized as a state of abnormal specific humoral and cell-mediated responses against constituents of body tissues. One time- honored approach to explaining the pathogenesis of autoimmunity has been application of the Koch's postulates, on loan from the field of microbiology suggesting that autoantibodies and/or autoreactive T cells are the presumed 'pathogens' of autoimmunity, and that passive transfer of these autoimmune factors to susceptible animals will result in the induction of the autoimmune disease. We suggest that autoimmunity is not in many cases due to the presence of factors leading to the autoimmune response in those susceptible. Instead, it is the lack of a factor which leads to the development of autoimmunity, a factor (cytokine, protein, gene, etc.) which is present in the healthy individual and normally protects in from disordered immune regulation. We propose to direct more research into therapeutic modulation of autoimmunity by administration of putative 'protective factors', rather than by attempts to depress or remove autoreactive cells and antibodies from the autoimmune.",
keywords = "Autoantibodies, Autoimmunity, Autoreactive cells, Pathogenesis",
author = "Chaim Putterman and Yaakov Naparstek",
year = "1999",
language = "English (US)",
volume = "47",
pages = "25--32",
journal = "Archivum Immunologiae et Therapiae Experimentalis",
issn = "0004-069X",
publisher = "Birkhauser Verlag Basel",
number = "1",

}

TY - JOUR

T1 - Koch's postulates and autoimmunity

T2 - An opposing viewpoint

AU - Putterman, Chaim

AU - Naparstek, Yaakov

PY - 1999

Y1 - 1999

N2 - Autoimmunity is characterized as a state of abnormal specific humoral and cell-mediated responses against constituents of body tissues. One time- honored approach to explaining the pathogenesis of autoimmunity has been application of the Koch's postulates, on loan from the field of microbiology suggesting that autoantibodies and/or autoreactive T cells are the presumed 'pathogens' of autoimmunity, and that passive transfer of these autoimmune factors to susceptible animals will result in the induction of the autoimmune disease. We suggest that autoimmunity is not in many cases due to the presence of factors leading to the autoimmune response in those susceptible. Instead, it is the lack of a factor which leads to the development of autoimmunity, a factor (cytokine, protein, gene, etc.) which is present in the healthy individual and normally protects in from disordered immune regulation. We propose to direct more research into therapeutic modulation of autoimmunity by administration of putative 'protective factors', rather than by attempts to depress or remove autoreactive cells and antibodies from the autoimmune.

AB - Autoimmunity is characterized as a state of abnormal specific humoral and cell-mediated responses against constituents of body tissues. One time- honored approach to explaining the pathogenesis of autoimmunity has been application of the Koch's postulates, on loan from the field of microbiology suggesting that autoantibodies and/or autoreactive T cells are the presumed 'pathogens' of autoimmunity, and that passive transfer of these autoimmune factors to susceptible animals will result in the induction of the autoimmune disease. We suggest that autoimmunity is not in many cases due to the presence of factors leading to the autoimmune response in those susceptible. Instead, it is the lack of a factor which leads to the development of autoimmunity, a factor (cytokine, protein, gene, etc.) which is present in the healthy individual and normally protects in from disordered immune regulation. We propose to direct more research into therapeutic modulation of autoimmunity by administration of putative 'protective factors', rather than by attempts to depress or remove autoreactive cells and antibodies from the autoimmune.

KW - Autoantibodies

KW - Autoimmunity

KW - Autoreactive cells

KW - Pathogenesis

UR - http://www.scopus.com/inward/record.url?scp=0032985260&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032985260&partnerID=8YFLogxK

M3 - Article

C2 - 11729825

AN - SCOPUS:0032985260

VL - 47

SP - 25

EP - 32

JO - Archivum Immunologiae et Therapiae Experimentalis

JF - Archivum Immunologiae et Therapiae Experimentalis

SN - 0004-069X

IS - 1

ER -