Methotrexate in rheumatoid arthritis: Studies with animal models

S. S. Kerwar, A. L. Oronsky

Research output: Contribution to journalArticle

Abstract

The present studies have shown that low doses of methotrexate can suppress the inflammation and joint destruction associated with animal models of arthritis. The antiinflammatory effects of methotrexate are probably related to its inhibitory effect on chemotaxis. At the low doses used, methotrexate does not induce systemic immunosuppression. In methotrexate-treated rats, an improvement in IL-2 synthesis is observed and increases in IL-2 levels are expected to improve cell mediated immunity. Suppressor cells appear to be very sensitive to methotrexate. Macrophage function is modulated by methotrexate. All of these effects including the effects on joint destruction are probably due to inhibition of DHFR activity of critical cells that are involved in the pathogenesis of rat arthritis induced either by adjuvant or by streptococcal cell walls. Some of these effects have been extended to human arthritis but additional studies are required to understand how low dose methotrexate exerts its beneficial effects in humans.

Original languageEnglish (US)
Pages (from-to)247-265
Number of pages19
JournalAdvances in Enzyme Regulation
Volume29
Issue numberC
DOIs
StatePublished - 1989
Externally publishedYes

Fingerprint

Methotrexate
Rheumatoid Arthritis
Animals
Animal Models
Arthritis
Interleukin-2
Rats
Joints
Cells
Experimental Arthritis
Macrophages
Chemotaxis
Cellular Immunity
Immunosuppression
Cell Wall
Anti-Inflammatory Agents
Inflammation

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

Cite this

Methotrexate in rheumatoid arthritis : Studies with animal models. / Kerwar, S. S.; Oronsky, A. L.

In: Advances in Enzyme Regulation, Vol. 29, No. C, 1989, p. 247-265.

Research output: Contribution to journalArticle

Kerwar, S. S. ; Oronsky, A. L. / Methotrexate in rheumatoid arthritis : Studies with animal models. In: Advances in Enzyme Regulation. 1989 ; Vol. 29, No. C. pp. 247-265.
@article{405b1268db044de2b12ee1470bb7ffae,
title = "Methotrexate in rheumatoid arthritis: Studies with animal models",
abstract = "The present studies have shown that low doses of methotrexate can suppress the inflammation and joint destruction associated with animal models of arthritis. The antiinflammatory effects of methotrexate are probably related to its inhibitory effect on chemotaxis. At the low doses used, methotrexate does not induce systemic immunosuppression. In methotrexate-treated rats, an improvement in IL-2 synthesis is observed and increases in IL-2 levels are expected to improve cell mediated immunity. Suppressor cells appear to be very sensitive to methotrexate. Macrophage function is modulated by methotrexate. All of these effects including the effects on joint destruction are probably due to inhibition of DHFR activity of critical cells that are involved in the pathogenesis of rat arthritis induced either by adjuvant or by streptococcal cell walls. Some of these effects have been extended to human arthritis but additional studies are required to understand how low dose methotrexate exerts its beneficial effects in humans.",
author = "Kerwar, {S. S.} and Oronsky, {A. L.}",
year = "1989",
doi = "10.1016/0065-2571(89)90105-2",
language = "English (US)",
volume = "29",
pages = "247--265",
journal = "Advances in Biological Regulation",
issn = "2212-4926",
publisher = "Elsevier BV",
number = "C",

}

TY - JOUR

T1 - Methotrexate in rheumatoid arthritis

T2 - Studies with animal models

AU - Kerwar, S. S.

AU - Oronsky, A. L.

PY - 1989

Y1 - 1989

N2 - The present studies have shown that low doses of methotrexate can suppress the inflammation and joint destruction associated with animal models of arthritis. The antiinflammatory effects of methotrexate are probably related to its inhibitory effect on chemotaxis. At the low doses used, methotrexate does not induce systemic immunosuppression. In methotrexate-treated rats, an improvement in IL-2 synthesis is observed and increases in IL-2 levels are expected to improve cell mediated immunity. Suppressor cells appear to be very sensitive to methotrexate. Macrophage function is modulated by methotrexate. All of these effects including the effects on joint destruction are probably due to inhibition of DHFR activity of critical cells that are involved in the pathogenesis of rat arthritis induced either by adjuvant or by streptococcal cell walls. Some of these effects have been extended to human arthritis but additional studies are required to understand how low dose methotrexate exerts its beneficial effects in humans.

AB - The present studies have shown that low doses of methotrexate can suppress the inflammation and joint destruction associated with animal models of arthritis. The antiinflammatory effects of methotrexate are probably related to its inhibitory effect on chemotaxis. At the low doses used, methotrexate does not induce systemic immunosuppression. In methotrexate-treated rats, an improvement in IL-2 synthesis is observed and increases in IL-2 levels are expected to improve cell mediated immunity. Suppressor cells appear to be very sensitive to methotrexate. Macrophage function is modulated by methotrexate. All of these effects including the effects on joint destruction are probably due to inhibition of DHFR activity of critical cells that are involved in the pathogenesis of rat arthritis induced either by adjuvant or by streptococcal cell walls. Some of these effects have been extended to human arthritis but additional studies are required to understand how low dose methotrexate exerts its beneficial effects in humans.

UR - http://www.scopus.com/inward/record.url?scp=0024812605&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024812605&partnerID=8YFLogxK

U2 - 10.1016/0065-2571(89)90105-2

DO - 10.1016/0065-2571(89)90105-2

M3 - Article

C2 - 2633612

AN - SCOPUS:0024812605

VL - 29

SP - 247

EP - 265

JO - Advances in Biological Regulation

JF - Advances in Biological Regulation

SN - 2212-4926

IS - C

ER -