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It’s not a bad thing to increase lymphatic vessel diameter

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CCL5 downregulates GLP-1 the ligand for GLP-1R, CCR5 upregulates GLP-1 (on the regulator list). I'm more familiar with GLP-1 in diabetes and NASH. But as you can see below the upregulation explains at least part of the reason maraviroc can clear tau and amyloid plaques, tighten the blood brain barrier and protect neurons.

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Previous studies have demonstrated that paravascular CSF recirculation and ISF solute clearance are dependent upon the polarized astroglial AQP4 water channel, which facilitates fluid movement between the perivascular and interstitial spaces. Widespread reactive astrogliosis (a large increase in and activity of astrocytes) post‐TBI (traumatic brain injury) is closely associated with the loss of perivascular AQP4 polarization.
Cerebral glucagon‐like peptide‐1 receptor activation alleviates traumatic brain injury by glymphatic system regulation in mice

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Astrogliosis is a response to an inflammatory state driven by overreaction of the immune system. Leronlimab would reverse that.

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Overall, these results indicate that TBI‐induced BBB disruption can be salvaged by cerebral GLP‐1R activation.

cerebral GLP‐1R activation effectively controlled TBI‐induced neuronal degeneration and apoptosis, thereby increasing the survival of neurons 3 days following TBI.

GLP‐1 was originally identified as a 31‐amino acid polypeptide secreted by L cells in the small intestine. It is also produced in the brain and plays neuroprotective roles by activating the GLP‐1 receptor. Studies have demonstrated that the number of amyloid beta and dense‐core plaques in the cortex of Alzheimer's mice model APP/PS1 mice treated with liraglutide (GLP‐1R agonist) decreased by 40%–50%, while the level of soluble amyloid oligomers decreased by 25%. 30 Our results demonstrated that cerebral GLP‐1R activation significantly increased paravascular fluid exchange and attenuated glymphatic system destruction post‐TBI.

In previous studies, Ex‐4 (artificial created ligand that activates (GLP-1R) was able to lower amyloid beta (1–42) induced oxidative stress and inflammation in astrocytes, demonstrating excellent neuroprotective effects. This could promote a reasonable hypothesis for cerebral GLP‐1R activation to improve the function of glymphatic system. Our results demonstrate that cerebral GLP‐1R activation can effectively ameliorate the reactive astrogliosis and loss of perivascular AQP4 polarization following TBI, thereby improving the transport function of glymphatic system.

In addition to the glymphatic pathway, the BBB also plays an important role in facilitating the transmission of neuroactive agents to maintain homeostasis of the brain microenvironment. BBB destruction, which occurs within hours or days following injury, is closely related to edema, neuroinflammation, and cell death. We demonstrated that cerebral GLP‐1R activation ameliorated TBI‐induced decrease of tight junction protein and microvessel coverage of collagen IV basement membrane, protecting the integrity and function of the BBB.

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