A chemokine that helps direct immune cells to sites of inflammation, mapped in a large Finnish cytokine study whose strongest hits sit right in the same signalling family the molecule itself belongs to.
MIP-1b (macrophage inflammatory protein 1-beta, also called CCL4) is a chemokine — a small signalling protein that helps direct immune cells, particularly monocytes and macrophages, toward sites of inflammation. Circulating levels of cytokines like this one vary substantially between people, and part of that variation is genetic.
Ahola-Olli et al. 2016 tested up to 8,293 Finnish participants across a panel of circulating cytokines and growth factors, finding 27 genome-wide-significant loci in total across the whole panel. Fifteen of the associated variants had expression quantitative trait loci (eQTL) evidence in whole blood — meaning the variant is statistically linked to how much of a nearby gene actually gets expressed, a real step toward a mechanism rather than a bare statistical association. The 35 variants on this page are the ones specifically tied to MIP-1b levels within that broader panel, not a separate study of this one molecule alone.
Two of them stand out as more biologically direct than the rest. rs113877493 sits in CCL4L1, a near-duplicate paralog gene of CCL4 — MIP-1b's own gene. rs79815064 sits in CCR3, a receptor for related CC-chemokines. A hit in the molecule's own duplicate gene and a hit in a receptor from the same signalling family are exactly the kind of result that makes a statistical association more credible — not a coincidence of an unrelated gene turning up by chance.
The study's authors also made a broader point worth stating: they linked cytokine-level variants like these to genetic risk loci already established for autoimmune diseases, including Crohn's disease, multiple sclerosis and ulcerative colitis — all three already covered elsewhere on this site. Circulating inflammation levels and autoimmune disease risk are not two separate genetic stories; they overlap.
MIP-1b is measured directly with a blood assay when it is clinically relevant, not inferred from genotype. Cytokine panels are used in specific clinical and research contexts (infection, autoimmune disease monitoring, some cancers); none of the 35 variants on this page is used to interpret them.
The genuinely useful part of this finding is mechanistic rather than actionable: it demonstrates that circulating levels of an inflammatory signalling molecule are shaped in part by common genetic variation, including variation right in the molecule's own gene family. That is a real contribution to understanding inflammation genetics generally, and to why autoimmune disease risk and cytokine-level genetics overlap — not a personal test result anyone should act on.
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about MIP-1b (CCL4) Levels comes down to these specific, well-studied positions — not a diagnosis. 79 positions are linked to this page; the ones this page's own text discusses are shown first.
Databases, guidelines and references
Not usefully for an individual. Each variant has a modest, population-level effect. MIP-1b is measured directly with a blood assay when it matters clinically, not inferred from genotype.
rs113877493 sits in CCL4L1, a near-duplicate gene of CCL4 (MIP-1b's own gene), and rs79815064 sits in CCR3, a receptor for related chemokines. Hits directly in a molecule's own gene family are more biologically credible than an association in an unrelated gene.
The discovery study's authors found that cytokine-level variants like these overlap with genetic risk loci already established for Crohn's disease, multiple sclerosis and ulcerative colitis — inflammation genetics and autoimmune disease genetics are not fully separate stories.
It is a chemokine — a signalling protein that helps direct immune cells, particularly monocytes and macrophages, toward sites of inflammation.
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