RhoH is important for positive thymocyte selection and T-cell receptor signaling

RhoH-deficient animals show impaired T-cell differentiation due to defective T-cell receptor signalling.

“On the other hand, animals showed impaired T-cell differentiation due to defective T-cell receptor signalling [21,28], as RhoH is necessary for the production and survival or migration of T-cells.”

RhoH is necessary for the production and survival or migration of T-cells.

“On the other hand, animals showed impaired T-cell differentiation due to defective T-cell receptor signalling [21,28], as RhoH is necessary for the production and survival or migration of T-cells.”

RhoH null mice are viable with no obvious defects in haematopoiesis, and RhoH is dispensable for development of myeloid, erythroid and B-cells.

“RhoH null mice are viable with no obvious defects in haematopoiesis and RhoH seems to be dispensable for the development of myeloid, erythroid and B-cells [28].”

RhoH-deficient mice do not develop lymphomas and have no obvious defects in HSC maintenance, but show impaired T-cell differentiation attributed to defective T-cell receptor signalling.

“RhoH-deficient mice did not develop lymphomas and had no obvious defects in HSC maintenance, but they showed impaired T-cell differentiation attributed to defective T-cell receptor signalling.”

RhoH-deficient mice show impaired development of thymocytes and reduced TCR signalling due to inefficient recruitment of Zap70.

“RhoH-deficient mice showed an impaired development of thymocytes and reduced TCR signalling due to inefficient recruitment of Zap70 [21,28].”

The phenotype of RhoH-deficient mice does not suggest a defect in maintenance of haematopoietic progenitors.

“However, the phenotype of the RhoH-deficient mice does not suggest that the mice have a defect in maintenance of haematopoietic progenitors [21,28].”

RhoH acts as a positive regulatory factor for thymocyte selection and T-cell receptor signalling.

“Two groups independently showed that RhoH acts as a positive regulatory factor for thymocyte selection and T-cell receptor signalling [21,28].”

The basal level of Rac1 activity is elevated in RhoH-deficient T-cells, suggesting RhoH is an antagonist for Rac1 activity by inhibiting basal Rac1 activity.

“However, the authors noted that the basal level of Rac1 activity seemed to be elevated in RhoH-deficient T-cells, suggesting once more that RhoH is an antagonist for Rac1 activity by inhibiting basal Rac1 activity [28].”

Regulation of LFA-1 mediated adherence by RhoH is not observed in T-lymphocytes.

“Recently, the Brakebusch group investigated whether regulation of LFA-1 mediated adherence by RhoH can also be observed in T-lymphocytes, but found that not to be the case [28].”

Despite reduced activation of Vav1, the activity of Rac1 and Rac2 is normal after TCR activation.

“Despite the reduced activation of Vav1, the activity of Rac1 and Rac2 were normal after TCR activation.”

RhoH contains a novel ITAM-like motif that serves as a binding site for Zap70, which is then shuttled to the T-cell receptor complex where it triggers activation of the LAT signalosome.

“RhoH contains a novel ITAM-like motif that serves as a binding site for Zap70, which is then shuttled to the T-cell receptor complex where it serves as a crucial molecule to trigger activation of the LAT signalosome.”

Phosphorylation of LAT, VAV1, PLCγ and Erk is reduced in RhoH-deficient DP cells.

“Indeed, phosphorylation of LAT, VAV1 and of PLCγ ανδ Erk, were reduced in RhoH-deficient DP cells [21,28].”

Dorn et al. found that RHOH is not required for TCR-induced activation of ZAP70, but is indispensable for the efficient interaction of ZAP70 with the LAT signalosome.

“Nevertheless, Dorn, T., et al. found that RHOH is not required for TCR-induced activation of ZAP70, but is indispensable for the e cient interaction of ZAP70 with the LAT signalosome (10).”