Sandbox Reserved 1647: Difference between revisions
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The transcription factor T-bet directs Th1 cell differentiation. The molecular mechanisms that underlie this lineage-specific gene regulation are not completely understood but several hypotheses have already been made on the action's mechanism of T-bet. <ref name="NFATc2 and T-bet contribute to T-helper-cell-subset-specific regulation of IL-21 expression">DOI 10.4049/jimmunol.1203403</ref> | The transcription factor T-bet directs Th1 cell differentiation. The molecular mechanisms that underlie this lineage-specific gene regulation are not completely understood but several hypotheses have already been made on the action's mechanism of T-bet. <ref name="NFATc2 and T-bet contribute to T-helper-cell-subset-specific regulation of IL-21 expression">DOI 10.4049/jimmunol.1203403</ref> | ||
We know that T-bet initiates Th1 lineage development from naive Thp cells by activating Th1 genetics and repressing the opposing Th2 programs. Th1 cells stimulate cellular immune response while Th2 stimulates humoral immune response and induces antibody production. <ref name="The Transcription Factor T-Bet Is Required for Optimal Type I Follicular Helper T Cell Maintenance During Acute Viral Infection">DOI 10.3389/fimmu.2019.00606</ref> | We know that T-bet initiates Th1 lineage development from naive Thp cells by activating Th1 genetics and repressing the opposing Th2 programs. Th1 cells stimulate cellular immune response while Th2 stimulates humoral immune response and induces antibody production. <ref name="The Transcription Factor T-Bet Is Required for Optimal Type I Follicular Helper T Cell Maintenance During Acute Viral Infection">DOI 10.3389/fimmu.2019.00606</ref> | ||
[[Image:TBET.jpg|thumb|upright=2 |T-bet action in the formation of SEC]] | [[Image:TBET.jpg|thumb|upright=2 |T-bet action in the formation of SEC]] | ||
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Recently, many studies have reported that T-bet also modulates other Th cell lineages, including [https://en.wikipedia.org/wiki/T_helper_17_cell Th17], [https://en.wikipedia.org/wiki/Regulatory_T_cell Treg], and follicular Th (TFH) cells, in coordination with many transcription factors, such as the retinoic acid-related orphan receptor-𝛾t [https://proteopedia.org/wiki/index.php/6b30 (ROR𝛾t)] <ref name="T-bet represses T(H)17 differentiation by preventing Runx1-mediated activation of the gene encoding RORγt">DOI 10.1038/ni.1969</ref>, runt-related transcription factor 3 [https://proteopedia.org/wiki/index.php/3mpm (RUNX3)], and B-cell lymphoma-6 [https://proteopedia.org/wiki/index.php/3lbz (BCL6)]. These findings suggest that T-bet is a transcription factor that is critical for fine-tuning Th cell development. | Recently, many studies have reported that T-bet also modulates other Th cell lineages, including [https://en.wikipedia.org/wiki/T_helper_17_cell Th17], [https://en.wikipedia.org/wiki/Regulatory_T_cell Treg], and follicular Th (TFH) cells, in coordination with many transcription factors, such as the retinoic acid-related orphan receptor-𝛾t [https://proteopedia.org/wiki/index.php/6b30 (ROR𝛾t)] <ref name="T-bet represses T(H)17 differentiation by preventing Runx1-mediated activation of the gene encoding RORγt">DOI 10.1038/ni.1969</ref>, runt-related transcription factor 3 [https://proteopedia.org/wiki/index.php/3mpm (RUNX3)], and B-cell lymphoma-6 [https://proteopedia.org/wiki/index.php/3lbz (BCL6)]. These findings suggest that T-bet is a transcription factor that is critical for fine-tuning Th cell development. | ||
=== TBX21 as an antiasthmatic regulator === | === TBX21 as an antiasthmatic regulator === | ||
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Researchers believe that the USP10-dependent T-bet deubiquitination and stabilization can regulate antigen induced immune disorder especially in Th1 specific inflammation. Thus, appropriate decreasing USP10 level may contribute to the T-bet degradation and inflammation attenuation. <ref name="Deubiquitination and stabilization of T-bet by USP10">DOI 10.1016/j.bbrc.2014.05.037</ref> | Researchers believe that the USP10-dependent T-bet deubiquitination and stabilization can regulate antigen induced immune disorder especially in Th1 specific inflammation. Thus, appropriate decreasing USP10 level may contribute to the T-bet degradation and inflammation attenuation. <ref name="Deubiquitination and stabilization of T-bet by USP10">DOI 10.1016/j.bbrc.2014.05.037</ref> | ||
Over the past few years, it has been shown by researchers that the polymorphism of TBX21 could act on nasal polyps and aspirin intolerance too. | Over the past few years, it has been shown by researchers that the polymorphism of TBX21 could act on nasal polyps and aspirin intolerance too. | ||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
