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Lupus an auto immune disease story. LL role?

The researchers worked backward, following the chain of events in the immune system and i dentified insufficient activity of a receptor in the T cells, a protein called aryl hydrocarbon, as a potential root cause of the disease.
Now, they’re studying whether a novel therapy could activate that receptor, leading the T cells to behave differently and, ultimately, through a cascade of events in the immune system, treat the autoimmune disease.

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From the original study -

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Type I interferon, a pathogenic driver of SLE, opposes AHR and JUN to promote T-cell production of CXCL13. These results place CXCL13+ TPH/TFH cells on a polarization axis opposite from T helper 22(TH22) cells and reveal AHR, JUN and interferon as key regulators of these divergent T-cell states.
Interferon subverts an AHR–JUN axis to promote CXCL13+ T-cells in lupus

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Leroblimab downregulates IFN-a (interferon alpha) type 1 interferon via BACH2 upregulation. The upshot is that IFN-a increases CXCL13 leading to an inflammatory state and autoimmune activation. CCR5 itself also adds to the inflammation and autoimmunity. Not only would leronlimab stop it's own activation of inflammation/autoimmunity but would reduce CXCL13 expression.

The researchers drug proposal most likely is targeting CXCL13. Which still leaves the panoply of responses from CCR5 to still activate the disease state. Leronlimab would take care of both CCR5 and CXCL13.