CD192 Flow Cytometry Antibody: Tracking CCR2 From Monocyte Recruitment to Organ Crosstalk
CD192 is the cluster-of-differentiation name for CCR2, and the two labels travel together in the literature. One describes an antigen, the other describes a receptor with a defined ligand set and a defined signaling output. A reagent for this target has to resolve a population defined by expression level rather than by lineage.
One Target, Two Species, Two Reagents
Two products cover this target, and they are not interchangeable. One is a mouse antibody against human CD192, clone S-2971. The other is a rat antibody against mouse CD192, clone S-R731. The distinction is practical rather than cosmetic. Human PBMC work needs the first, and mouse disease models, including the chimera experiments described below, need the second.
Cross-reactivity should be verified rather than assumed. The extracellular loops of chemokine receptors diverge quickly between species. A reagent validated on human cells may therefore fail on mouse tissue, even when the intracellular domains are conserved.
Receptor Architecture and Ligand Set
CCR2 is a seven-transmembrane G protein-coupled receptor of the beta-chemokine receptor family. It is displayed on monocytes, macrophages, basophils, dendritic cells and a subset of T cells. The ligand set is broad within the MCP group: CCL2/MCP-1, CCL8/MCP-2, CCL7/MCP-3 and CCL13/MCP-4.
Occupancy triggers G protein dissociation and several parallel cascades. Adenylyl cyclase is inhibited, which lowers cAMP and relieves PKA restraint. JAK2/3 phosphorylates STAT. PI3K feeds Akt, mTOR, IKK and NF-kappaB. Ras recruits Raf and MEK1 to ERK1/2, p38 and JNK, while PLC generates IP3 and releases calcium.
CCR2 signaling cascade from extracellular CCL2 binding through G protein coupled branches including cAMP/PKA, JAK-STAT, PI3K-Akt, Ras-Raf-MEK-ERK and PLC-IP3-calcium, converging on nuclear programs for survival, migration and cytokine production
The nuclear output is a coordinated program of survival, migration, apoptosis, cytokine production and growth. That breadth explains why CCR2 blockade produces different results in different models. The receptor is not a single switch but a hub with several downstream branches.
Why Acute Kidney Injury Reaches the Aorta
Acute kidney injury is a rapid loss of the kidney's capacity to clear metabolic waste. Azotemia, electrolyte disturbance and acid-base imbalance follow. It is common in hospitalized and critically ill patients, and the prognosis is poor. Two long-term endpoints dominate: chronic kidney disease and cardiovascular disease.
Registry data show a positive association between AKI and cardiovascular events, and between AKI and mortality. The association alone does not explain mechanism. Persistent inflammation at the injury site is the leading candidate, because inflammatory leukocytes drive atherogenesis.
The Experimental Chain in Detail
In May 2022 a team at Hannover Medical School published a study in the Journal of the American Society of Nephrology that made the link explicit. Each step of the design removes one alternative explanation.
Unilateral renal ischemia-reperfusion was performed in LDL receptor knockout mice. Ten weeks of high-fat diet produced measurable atherosclerosis in the aortic arch. Injured animals developed more extensive plaque, with heavy deposition of CD11b-positive macrophages and antigen-presenting cells.
Aortic gene arrays then showed specific upregulation of chemokine and T cell related genes, which pointed to a remote inflammatory program rather than local spillover. Single-cell sequencing of the injured kidney identified the source. Inflammatory cell types expanded after injury, and the differentially expressed aortic inflammatory genes were highest in kidney leukocytes.
Ccl2 rose most among those genes, and most Ccl2-expressing cells also expressed Ccr2. CCL2 peaked early, at three weeks, while CCR2 rose steadily to ten weeks. Flow cytometry confirmed continuous leukocyte enrichment in the injured kidney.
Bone marrow chimeras completed the argument. Ccr2 heterozygous chimeras showed an increased proportion of normal leukocytes in kidney relative to spleen and aorta after injury, a pattern absent in untreated mice. Homozygous knockout chimeras showed reduced expression of the inflammation genes that normally persist in the aorta, and atherosclerosis after injury was significantly attenuated.
Inflammatory and Resident Monocytes Are Not One Population
CCR2 is high on inflammatory monocytes and low on resident monocytes. A gate drawn on CCR2 alone therefore mixes two populations with different origins and different fates. Ly6C separates them in mouse blood, and the human equivalent requires additional markers plus a stated gating order.
This is also where the therapeutic literature becomes confusing. CCR2 antagonists and blocking antibodies change the ratio as well as the total, and a total-count readout can miss the effect entirely. Report both the frequency and the mean fluorescence intensity, and name the population each value refers to.
Applications in Practice
Five uses follow directly from the biology. Subset analysis distinguishes inflammatory from resident monocytes. Organ crosstalk studies track CCR2-positive cells across tissues after kidney injury. Disease model work quantifies infiltration in atherosclerosis and rheumatoid arthritis.
Therapeutic monitoring tests whether a CCR2 antagonist or blocking antibody reduced recruitment. Bone marrow chimera work separates donor-derived from recipient-derived cells by CCR2 expression. Each application needs the species-matched reagent described above, and each benefits from reporting the parent monocyte gate alongside the CCR2 result.
Cell handling deserves a note. Chemokine receptors internalize after ligand binding, so a prolonged digestion or a warm dissociation step can strip surface CCR2 and flatten the signal. Keep samples cold and stain early.
Reporting Standards for a CCR2 Claim
A CCR2 result is easy to overstate because the marker is continuous rather than binary. Report the parent gate, the Ly6C split, the percentage within each subset and the mean fluorescence intensity. State the clone and the species of the sample, since the two reagents above target different molecules in different hosts.
Where a blocking antibody or antagonist is part of the design, measure receptor occupancy separately from receptor expression. A fall in signal can mean reduced transcription, receptor internalization or epitope masking by the blocking reagent, and those three have different implications for the mechanism.
Product Information
The two reagents are species-matched rather than duplicated, so the table separates them by host and reactivity. Catalog numbers remain plain text.
| Product Name | Catalog No. | Host and Reactivity | Clone | Application |
|---|---|---|---|---|
| Mouse Anti-Human CD192 Antibody (S-2971) | S0B8458 | Mouse anti-human | S-2971 | Flow cytometry |
| Rat Anti-Mouse CD192 Antibody (S-R731) | S0B5295 | Rat anti-mouse | S-R731 | Flow cytometry |
Both products are supplied for research use only and are not intended for diagnostic or therapeutic procedures.
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