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LRRC32
SNP Table
| variant | genotype | frequency | risk allele |
|---|---|---|---|
| rs960855928 | |||
| rs115658755 | |||
| rs116043188 | |||
| rs138705487 | |||
| rs139661666 | |||
| rs140733002 | |||
| rs1408286302 | |||
| rs142698633 | |||
| rs142940671 | |||
| rs143082901 | |||
| rs145077681 | |||
| rs145156630 | |||
| rs148695421 | |||
| rs150096749 | |||
| rs150588636 | |||
| rs182036426 | |||
| rs201131944 | |||
| rs201222193 | |||
| rs201293120 | |||
| rs201402758 |
Find on This Page
Summary
LRRC32 codes for GARP, a protein that promotes the development of pro-inflammatory immune cells by aiding in TGF-beta activation. A variant of LRRC32 may play a role in alopecia areata by increasing the production of GARP and excessively activating TGF-beta.
Lifestyle and supplement modifications may counteract the effects of this variant by decreasing TGF-beta activity.
Protein names
Found in These Blog Articles
More Information
The LRRC32 gene codes for GARP, a protein that promotes the activation of TGF-beta. More specifically, GARP is found on the surfaces of regulatory T cells (Tregs), where activation of TGF-beta has been shown to alter Treg activity [R, R, R].
While Tregs are well-known for their ability to prevent inflammation and autoimmune (self-targeting) reactions, TGF-beta combined with IL-6 may stimulate their conversion to pro-inflammatory Th17 cells [R].
In people with the autoimmune disorder alopecia areata (spot baldness), TGF-beta and IL-6 are elevated, and the ratio of Th17 cells to Tregs is biased toward Th17. In fact, higher levels of Th17 immune messengers (cytokines) have been linked to increased severity of alopecia areata [R, R, R, R].
Furthermore, greater TGF-beta activity in hair follicles has been suggested to shorten hair growth cycles, ultimately leading to hair loss [R].
A variant of LRRC32 has been associated with alopecia areata. While the mechanism has not yet been elucidated, it’s possible that this variant may increase the production of GARP, thereby inducing excessive activation of TGF-beta and promoting the development of Th17 cells [R].
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