Abstract
There is accumulated evidence suggesting that a polyclonal B cell activation is a primary etiologic defect of autoimmune diseases in both mice and humans. Based on this previous finding, the influence of various antiarthritic agents on lipopolysaccharide-induced B cell colony formation in mouse spleen cells was studied. When added to cell culture, aurothioglucose, chloroquine, and prostaglandin E1 had a suppressive effect on B cell colony formation at clinically relevant concentrations. A 50% suppression was obtained at 10-7 to 10-8 M for aurothioglucose, 10-7 M for chloroquine, and 10-7 to 10-8 M for prostaglandin E1, respectively. All of the immunosuppressive drugs and glucocorticoids examined decreased the number of colonies with a variety of intensity. Nonsteroidal antiinflammatory drugs have only a slight inhibitory effect at high concentrations. Both penicillamine and levamisole had no effect on B cell colony formation. This experimental system might be useful in searching for new and unique drugs and in evaluating the mode of action of drugs used against autoimmune diseases.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1-7 |
| Number of pages | 7 |
| Journal | Immunopharmacology |
| Volume | 7 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1984 |
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Keywords
- Antiarthritic drugs
- Autoimmunity
- B cell colony formation
ASJC Scopus subject areas
- Pharmacology
Cite this
Inhibition by various antiarthritic agents of murine splenic B cell colony formation. / Ohsugi, Yoshiyuki; Gershwin, M. Eric.
In: Immunopharmacology, Vol. 7, No. 1, 1984, p. 1-7.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inhibition by various antiarthritic agents of murine splenic B cell colony formation
AU - Ohsugi, Yoshiyuki
AU - Gershwin, M. Eric
PY - 1984
Y1 - 1984
N2 - There is accumulated evidence suggesting that a polyclonal B cell activation is a primary etiologic defect of autoimmune diseases in both mice and humans. Based on this previous finding, the influence of various antiarthritic agents on lipopolysaccharide-induced B cell colony formation in mouse spleen cells was studied. When added to cell culture, aurothioglucose, chloroquine, and prostaglandin E1 had a suppressive effect on B cell colony formation at clinically relevant concentrations. A 50% suppression was obtained at 10-7 to 10-8 M for aurothioglucose, 10-7 M for chloroquine, and 10-7 to 10-8 M for prostaglandin E1, respectively. All of the immunosuppressive drugs and glucocorticoids examined decreased the number of colonies with a variety of intensity. Nonsteroidal antiinflammatory drugs have only a slight inhibitory effect at high concentrations. Both penicillamine and levamisole had no effect on B cell colony formation. This experimental system might be useful in searching for new and unique drugs and in evaluating the mode of action of drugs used against autoimmune diseases.
AB - There is accumulated evidence suggesting that a polyclonal B cell activation is a primary etiologic defect of autoimmune diseases in both mice and humans. Based on this previous finding, the influence of various antiarthritic agents on lipopolysaccharide-induced B cell colony formation in mouse spleen cells was studied. When added to cell culture, aurothioglucose, chloroquine, and prostaglandin E1 had a suppressive effect on B cell colony formation at clinically relevant concentrations. A 50% suppression was obtained at 10-7 to 10-8 M for aurothioglucose, 10-7 M for chloroquine, and 10-7 to 10-8 M for prostaglandin E1, respectively. All of the immunosuppressive drugs and glucocorticoids examined decreased the number of colonies with a variety of intensity. Nonsteroidal antiinflammatory drugs have only a slight inhibitory effect at high concentrations. Both penicillamine and levamisole had no effect on B cell colony formation. This experimental system might be useful in searching for new and unique drugs and in evaluating the mode of action of drugs used against autoimmune diseases.
KW - Antiarthritic drugs
KW - Autoimmunity
KW - B cell colony formation
UR - http://www.scopus.com/inward/record.url?scp=0021725158&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0021725158&partnerID=8YFLogxK
U2 - 10.1016/0162-3109(84)90002-X
DO - 10.1016/0162-3109(84)90002-X
M3 - Article
C2 - 6425240
AN - SCOPUS:0021725158
VL - 7
SP - 1
EP - 7
JO - Immunopharmacology
JF - Immunopharmacology
SN - 0162-3109
IS - 1
ER -