Phenotypes of STAT knock-out mice
| STAT . | Cytokine affected . | Knockout phenotype . |
|---|---|---|
| STAT1 | IFN-α/β, γ | Defective IFN-dependent immune responses |
| High susceptibility to bacterial/viral infections13 14 | ||
| STAT2 | IFN-α/β | Defective type I IFN-dependent immune responses15 |
| STAT3 | IL-2, IL-6, IL-7, IL-9, IL-10, IL-11, IL-15, IL-21, EGF, OSM, G-CSF*, TPO, LIF, GH | Early fetal death16 17 Impaired T-cell proliferation in response to IL-618 and IL-219† |
| Impaired IL-10–mediated anti-inflammatory responses20‡ | ||
| Defective wound healing in skin211-153 | ||
| Delayed involution of mammary gland after weaning221-155 | ||
| STAT4 | IL-12 | Impaired Th1 cell development23 24 |
| STAT5a and/or STAT5b | IL-2*, IL-3, IL-5, IL-7, IL-9, IL-15, G-CSF, GM-CSF, EPO, TPO, GH, PRL | Loss of mammary gland development and lactogenesis251-154 Loss of sexually dimorphic growth in males261-154 |
| Defective granulocyte proliferation in response to GM-CSF27# | ||
| Impaired cell growth in response to IL-228 29 1-160 | ||
| Defective natural killer (NK) cell development291-160 | ||
| Infertility in females301-164 | ||
| Fetal anemia311-164 | ||
| Reduced number of NK cells and impaired IL-2–induced T-cell proliferation321-164 | ||
| STAT6 | IL-4, IL-13 | Impaired Th2 differentiation, defective IgE class switch33-36 |
| STAT . | Cytokine affected . | Knockout phenotype . |
|---|---|---|
| STAT1 | IFN-α/β, γ | Defective IFN-dependent immune responses |
| High susceptibility to bacterial/viral infections13 14 | ||
| STAT2 | IFN-α/β | Defective type I IFN-dependent immune responses15 |
| STAT3 | IL-2, IL-6, IL-7, IL-9, IL-10, IL-11, IL-15, IL-21, EGF, OSM, G-CSF*, TPO, LIF, GH | Early fetal death16 17 Impaired T-cell proliferation in response to IL-618 and IL-219† |
| Impaired IL-10–mediated anti-inflammatory responses20‡ | ||
| Defective wound healing in skin211-153 | ||
| Delayed involution of mammary gland after weaning221-155 | ||
| STAT4 | IL-12 | Impaired Th1 cell development23 24 |
| STAT5a and/or STAT5b | IL-2*, IL-3, IL-5, IL-7, IL-9, IL-15, G-CSF, GM-CSF, EPO, TPO, GH, PRL | Loss of mammary gland development and lactogenesis251-154 Loss of sexually dimorphic growth in males261-154 |
| Defective granulocyte proliferation in response to GM-CSF27# | ||
| Impaired cell growth in response to IL-228 29 1-160 | ||
| Defective natural killer (NK) cell development291-160 | ||
| Infertility in females301-164 | ||
| Fetal anemia311-164 | ||
| Reduced number of NK cells and impaired IL-2–induced T-cell proliferation321-164 | ||
| STAT6 | IL-4, IL-13 | Impaired Th2 differentiation, defective IgE class switch33-36 |
IFN indicates interferon; IL, interleukin; OSM, oncostatin M; G, granulocyte; GM, granulocyte/macrophage; CSF, colony-stimulating factor; TPO, thrombopoietin; LIF, leukemia inhibitory factor; GH, growth hormone; and PRL, prolactin.
More prominent.
T-cell–selective STAT3 knockout mice.
Macrophage-selective STAT3 knockout mice.
Keratinocyte-selective STAT3 knockout mice.
Mammary gland epithelium-selective STAT3 knockout mice.
STAT5a only.
#STAT5b only.
More prominent in STAT5b.
STAT5a/STAT5b double knock out.