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CCL19 and Tuberculosis

Two independent transcriptomic studies have demonstrated that CCL19 (HGNC:10617) is differentially expressed in tuberculosis (MONDO_0018076). In one study involving HIV-positive individuals, CCL19 expression was significantly altered between active TB cases (n = 29 [PMID:27553407]) and TST-negative patients, while a second study reported differential expression across 43 active TB patients compared to latent TB cases (n = 43 active [PMID:33472618]). These findings suggest that CCL19 expression may serve as a molecular marker to discriminate between active and latent tuberculosis infections.

Despite the reproducible expression differences observed in these cohorts, there is no evidence of causative rare variants or familial segregation supporting a direct genetic role of CCL19 in TB susceptibility. Furthermore, direct functional studies linking CCL19 to the molecular pathogenesis of tuberculosis remain lacking. Additional research, particularly involving variant-level and mechanistic analyses, is warranted to solidify the clinical utility of CCL19 as a diagnostic biomarker. Key take‑home sentence: Although current evidence is limited to transcriptomic differences, CCL19 holds promise as a diagnostic marker for tuberculosis in at‑risk populations.

References

  • Tuberculosis (Edinburgh, Scotland) • 2016 • Discriminative expression of whole blood genes in HIV patients with latent and active TB in Ethiopia PMID:27553407
  • Respiratory research • 2021 • Gene expression pattern analysis using dual‑color RT‑MLPA and integrative genome‑wide association studies of eQTL for tuberculosis susceptibility PMID:33472618

Evidence Based Scoring (AI generated)

Gene–Disease Association

Limited

Differential expression observed in two independent cohorts (29 active TB cases [PMID:27553407] and 43 active TB cases [PMID:33472618]) without supportive variant or segregation evidence.

Genetic Evidence

Limited

Two independent transcriptomic studies demonstrate dysregulated CCL19 expression in tuberculosis cases; however, there is a lack of variant-level associations or familial segregation data.

Functional Evidence

Limited

No direct functional studies link CCL19 to tuberculosis pathogenesis; available data are limited to correlative gene expression differences.