Abstract
Inhibitory receptors originally identified in natural killer (NK) cells have also been detected m other leukocyte types, thus suggesting that they may play a more general rote in the control of leukocyte function. Here we report data on p75/adhesion receptor molecule 1 (AIRM1), a surface inhibitory receptor of the sialoadhesin family originally identified in NK cells that is also expressed by normal and leukemic myeloid cells. Given the homology between p75/AIRM1 and CD33, we also reanalyzed CD33, a major myeloid marker of still unknown function. We discuss recent data indicating that engagement of p75/AIRM1 or CD33 sharply inhibits the in vitro proliferation/differentiation of CD34+ myeloid precursors induced by stem cell factor and granulocyte-macrophage colony-stimulating factor. Importantly, a similar in vitro inhibitory effect occurs in monocyte/macrophages as well as in chronic or acute myeloid leukemias. While CD33 appears to act via the induction of apoptosis, p75/AIRM1 blocks cell proliferation but does not appear to induce apoptosis. A synergistic effect in the induction of apoptosis has also been documented between antibodies specific for CD33 and the chemotherapic agent etoposide, Taken together, the use of appropriate ligands against CD33 or p75/AIRM1 may represent a new therapeutic tool for treatment of myeloid leukemias or diseases characterized by overwhelming macrophage activation.
| Original language | English |
|---|---|
| Pages (from-to) | 260-268 |
| Number of pages | 9 |
| Journal | Immunological Reviews |
| Volume | 181 |
| DOIs | |
| Publication status | Published - 2001 |
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ASJC Scopus subject areas
- Immunology
Cite this
p75/AIRM1 and CD33, two sialoadhesin receptors that regulate the proliferation or the survival of normal and leukemic myeloid cells. / Mingari, Maria Cristina; Vitale, Chiara; Romagnani, Chiara; Falco, Michela; Moretta, Lorenzo.
In: Immunological Reviews, Vol. 181, 2001, p. 260-268.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - p75/AIRM1 and CD33, two sialoadhesin receptors that regulate the proliferation or the survival of normal and leukemic myeloid cells
AU - Mingari, Maria Cristina
AU - Vitale, Chiara
AU - Romagnani, Chiara
AU - Falco, Michela
AU - Moretta, Lorenzo
PY - 2001
Y1 - 2001
N2 - Inhibitory receptors originally identified in natural killer (NK) cells have also been detected m other leukocyte types, thus suggesting that they may play a more general rote in the control of leukocyte function. Here we report data on p75/adhesion receptor molecule 1 (AIRM1), a surface inhibitory receptor of the sialoadhesin family originally identified in NK cells that is also expressed by normal and leukemic myeloid cells. Given the homology between p75/AIRM1 and CD33, we also reanalyzed CD33, a major myeloid marker of still unknown function. We discuss recent data indicating that engagement of p75/AIRM1 or CD33 sharply inhibits the in vitro proliferation/differentiation of CD34+ myeloid precursors induced by stem cell factor and granulocyte-macrophage colony-stimulating factor. Importantly, a similar in vitro inhibitory effect occurs in monocyte/macrophages as well as in chronic or acute myeloid leukemias. While CD33 appears to act via the induction of apoptosis, p75/AIRM1 blocks cell proliferation but does not appear to induce apoptosis. A synergistic effect in the induction of apoptosis has also been documented between antibodies specific for CD33 and the chemotherapic agent etoposide, Taken together, the use of appropriate ligands against CD33 or p75/AIRM1 may represent a new therapeutic tool for treatment of myeloid leukemias or diseases characterized by overwhelming macrophage activation.
AB - Inhibitory receptors originally identified in natural killer (NK) cells have also been detected m other leukocyte types, thus suggesting that they may play a more general rote in the control of leukocyte function. Here we report data on p75/adhesion receptor molecule 1 (AIRM1), a surface inhibitory receptor of the sialoadhesin family originally identified in NK cells that is also expressed by normal and leukemic myeloid cells. Given the homology between p75/AIRM1 and CD33, we also reanalyzed CD33, a major myeloid marker of still unknown function. We discuss recent data indicating that engagement of p75/AIRM1 or CD33 sharply inhibits the in vitro proliferation/differentiation of CD34+ myeloid precursors induced by stem cell factor and granulocyte-macrophage colony-stimulating factor. Importantly, a similar in vitro inhibitory effect occurs in monocyte/macrophages as well as in chronic or acute myeloid leukemias. While CD33 appears to act via the induction of apoptosis, p75/AIRM1 blocks cell proliferation but does not appear to induce apoptosis. A synergistic effect in the induction of apoptosis has also been documented between antibodies specific for CD33 and the chemotherapic agent etoposide, Taken together, the use of appropriate ligands against CD33 or p75/AIRM1 may represent a new therapeutic tool for treatment of myeloid leukemias or diseases characterized by overwhelming macrophage activation.
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UR - http://www.scopus.com/inward/citedby.url?scp=0034904570&partnerID=8YFLogxK
U2 - 10.1034/j.1600-065X.2001.1810122.x
DO - 10.1034/j.1600-065X.2001.1810122.x
M3 - Article
C2 - 11513147
AN - SCOPUS:0034904570
VL - 181
SP - 260
EP - 268
JO - Immunological Reviews
JF - Immunological Reviews
SN - 0105-2896
ER -