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CXCL9/CXCL10-CXCR3 signaling axis

Candidate: concept label1 source documents6 linked claims
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Aliases

CXCL9/10 signaling, CXCR3 signaling

Extracted Explainers

What the tool is doing

This paper studies persistent IFNγ-driven CXCL9/CXCL10 signaling as a contributor to nociceptor sensitization in HIV-DSP models. The axis is linked to TRPV1 induction in sensory neurons and includes CXCR3 as the reported receptor for CXCL9/10.

Source 1DOIPubMed

What problem it solves

It offers a candidate upstream mechanism for why nociceptive signaling may persist in HIV-DSP despite ART.

Source 1DOIPubMed

What it does not solve

The abstract does not show that CXCR3 blockade explains the conditioned-media effect, so the full mediator of macrophage-conditioned signaling remains unresolved.

Source 1DOIPubMed

Alternatives

The abstract contrasts IFNγ-driven signaling with LPS-related pathway activity and reports that LPS did not stimulate macrophages to release CXCL9/CXCL10 in the parallel experiment.

Source 1DOIPubMed

Evidence Snippets

the IFNγ-inducible chemokines CXCL9 and CXCL10 remained significantly upregulated... pharmacological inhibition of CXCR3, the receptor of CXCL9/10
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1cell responsesupports2026Source 1DOIPubMed

IFNγ but not LPS stimulated monocyte-derived macrophages to release CXCL9 and CXCL10.

Quoted textsource-backed
IFNγ but not LPS stimulated monocyte-derived macrophages (MDMs) to release CXCL9 and CXCL10.
Claim 2conditioned media effectsupports2026Source 1DOIPubMed

Conditioned media from IFNγ-treated monocyte-derived macrophages modestly increased TRPV1 expression in iPSC-derived peripheral sensory neurons.

Quoted textsource-backed
Conditioned media from IFNγ-treated MDMs modestly increased TRPV1 expression in iPSC-PSNs
Claim 3differential expressionsupports2026Source 1DOIPubMed

ART reduced overall IFNγ and LPS pathway activity, but CXCL9 and CXCL10 remained significantly upregulated.

Quoted textsource-backed
Although ART reduced overall IFNγ and LPS pathway activity, the IFNγ-inducible chemokines C-X-C motif chemokine ligand (CXCL)9 and CXCL10 remained significantly upregulated.
Claim 4expression changesupports2026Source 1DOIPubMed

CXCL9 and CXCL10 treatment increased TRPV1 expression but not TRPA1 expression in iPSC-derived peripheral sensory neurons.

Quoted textsource-backed
we treated induced pluripotent stem cell-derived peripheral sensory neurons (iPSC-PSNs) with CXCL9 and CXCL10, which induced a significant increase in TRPV1 but not TRPA1 expression
Claim 5mechanistic interpretationsupports2026Source 1DOIPubMed

Persistent IFNγ-driven CXCL9/10 signaling may contribute to nociceptor sensitization underlying HIV-associated distal sensory polyneuropathy even in the presence of ART.

Quoted textsource-backed
Together, these data indicate that persistent IFNγ-driven CXCL9/10 signaling may be one contributor to nociceptor sensitization underlying HIV-DSP, even in the presence of ART.
Claim 6pharmacological perturbationsupports2026Source 1DOIPubMed

Pharmacological inhibition of CXCR3 did not reduce the conditioned-media-induced increase in TRPV1 expression in iPSC-derived peripheral sensory neurons.

Quoted textsource-backed
pharmacological inhibition of CXCR3, the receptor of CXCL9/10, did not reduce this effect