Differential dendritic cell expression in chronic inflammatory arthritis: implications for their maturation, recruitment and involvement in disease

Dendritic cells (DC) from both myeloid and lymphoid haematopoietic lineages comprise a complex network of professional antigen-presenting cells, directly linking innate and adaptive immunity. Although implicated in the pathogenesis of inflammatory arthritides, their subset analysis has been hampered by a lack of specific DC markers and reliable quantitation.

The study was conducted to quantify circulating plasmacytoid DC (pDC) and myeloid DC (mDC) populations in different chronic inflammatory arthritides utilizing a novel assay involving the DC-specific markers BDCA-1 and BDCA-2.

Peripheral blood (PB) was obtained from RA (n = 12), PsA (n = 13), AS (n = 11) and healthy donors (n = 12). Synovial fluids (SF) were also examined from a subset of PB samples (4 RA, 2 PsA, 1 AS). A white blood count (WBC) was performed on all samples, followed by DC enumeration using the blood DC enumeration kit (Miltenyi Biotec).

Circulating PB mDC populations were significantly decreased in RA patients (P = 0.004), but not in PsA or AS patients, compared with healthy donors (normal = 175 × 10², RA = 95.5 × 10², PsA = 141 × 10², AS = 152 × 10²). Circulating PB pDC populations were significantly decreased in RA (P = 0.01) and PsA (P = 0.01) but not AS patients (normal = 137 × 10², RA = 54.6 × 10², PsA = 69.5 × 10², AS = 104 × 10²). The mDC : pDC ratio in PB of all patient groups was similar to that in healthy donors, whereas mDC exceeded pDC in SF in all patient cohorts analyzed (RA 6.6 : 1, PsA 7.35 : 1 and AS 100 : 1).

We report the ex vivo tracking of circulating pDC and mDC populations, revealing significantly reduced numbers of pDC in RA and PsA and mDC in RA patients. mDC subsets appear to be the predominant population in SF in all patient cohorts studied. Understanding the biology of DC subsets in chronic inflammatory arthritis will elucidate their presumed critical role at the interface of innate and acquired (autoreactive) immune responses.