Review Article
Role of PIR-B in Autoimmune Glomerulonephritis
Table 1
Phenotypes observed in
mice and
Pirb transgenic (tg) mice.
| Mice | Cells | Phenotypes | References |
| Pirb -/- | B-2 cells | Enhanced proliferation upon BCR stimulation | [10] | B-1 cells | Enhanced proliferation and autoantibody production upon CpG stimulation | [11] | DCs | Impaired maturation | [10] | | Exacerbated graft-versus-host disease | [12] | CD8+ T cells | Augmented activation | [13] | Mast cells | Augmented anaphylaxis | [14] | Macrophages | Augmented cytokine and chemokine signaling | [15] | Neutrophils | Augmented integrin signaling | [16] | Eosinophils | Enhanced recruitment in Th2 response | [17] | Macrophages | Sensitive to Salmonella infection | [18] | Macrophages | Reduced binding of Staphylococcus aureus | [19] | Neuronal cells | Enhanced plasticity of visual nerve connections | [20] | | Enhanced neurite outgrowth | [21] | Pirb tg | Thymocytes | Normal development | [22] | Mature T cells | Impaired Th1 response | [22] |
|
|
Cells involved mainly in the observed phenotype. Major phenotypes observed. Unidentified, though involving macrophages.
|