Table 1.
Knock-out mice of Ig Sf molecules presenting haematopoietic defects.
| Adhesion molecule | Year | Ligands | Altered phenotype | Haematopoietic phenotype | References |
|---|---|---|---|---|---|
| ICAM-1 | 1994 | αLβ2 | cardiovascular, cellular, digestive/alimentary, growth/size/body, haematopoietic, homeostasis, immune, mortality/aging, neoplasm, vision/eye | Expansion of Lt-HSC compartment associated with impaired quiescence and myeloid expansion | (69, 70) |
| VCAM-1 | 1995 | α4β1 | cardiovascular, embryo, growth/size/body, homeostasis, mortality/aging, haematopoietic | Increased frequencies of circulating progenitors | (65, 71) |
| α4β7 | |||||
| ESAM | 2003 | ESAM | cardiovascular, cellular, growth/size/body, haematopoietic, immune | Increased HSCs frequency and proliferation compared to wild-type mice | (63, 72) |
| ALCAM (CD166) | 2004 | ALCAM | nervous system, vision/eye, haematopoietic | Defects in Lt-HSC engraftment although no differences in absolute numbers of HSCs were observed | (61, 73, 74) |
| CD6 | |||||
| JAM-C | 2004 | JAM-C | behaviour, cardiovascular, cellular, craniofacial, digestive/alimentary, endocrine/exocrine, growth/size/body, haematopoietic, immune, integument, mortality/aging, nervous system, reproductive, respiratory, skeleton | Increased number of CMPs | (75–77) |
| JAM-B | |||||
| αMβ2 | |||||
| JAM-B | 2011 | JAM-C | haematopoietic, homeostasis, mortality/aging, skeleton | Loss of quiescent HSCs and exacerbated response to mobilizing agent | (78) |
| α4β1 |