Background and objectives: Composition of the peripheral blood (PB) cell populations and their activation state reflect the immune status of a patient. Rheumatoid arthritis (RA) is characterized by abnormal B- and T-cell functions. The objective of this study was to assess the profiles of the PB mononuclear cell (PBMC) populations in patients with rheumatoid and osteoarthritis (OA) in comparison with healthy control (HC) subjects in order to evaluate the PBMC profiles as a potential diagnostic characteristic in RA. The second aim was to assess the CCR1 and CCR2 expression on PB lymphocytes and correlate it with the plasma levels of matrix metallopeptidase 9 (MMP-9), IL-17F, TNF-α, IL-6, and IL-10. Materials and Methods: The frequency and phenotype, including CCR1 and CCR2, of the PBMC populations (monocytes, CD19⁺B cells, and T/NK lymphocytes) in RA (n = 15) and OA (n = 10) patients and HC (n = 12) were analyzed by five-color flow cytometry. DNA of the viruses, HHV-6, HHV-7, and B19, in the whole blood and cell-free plasma, were assessed by nested-polymerase chain reaction (PCR). Results: Active persistent or acute infections, caused by HHV-6, HHV-7, or B19, were not detected in patients of this study. Both CCR1 and CCR2 were determined on the PB B and T/NK lymphocytes in several RA and OA patients and HCs. However, in patients, the frequency of the CCR1-positive T/NK lymphocytes showed a weak negative correlation with the IL-10 level, while the frequency of the CCR2-positive B cells correlated positively with the level of IL-6. Statistically significant differences in the proportions of the CD19-positive and CD19-negative lymphocyte and monocyte subsets within the PBMC set were determined between RA and OA patients and HC adults. Conclusions: We have shown in our pilot study with rather small cohorts of patients that the PBMC-population profiles were very consistent, and statistically significantly differed between RA and OA patients and HC subjects.

Klippel–Trenaunay–Weber syndrome is a rare syndrome; unfortunately, very few studies of the connection between hypersplenism, nephrotic syndrome, and Klippel–Trenaunay–Weber syndrome have been published. We report the case of a 40-year-old white man with a typical clinical presentation of Klippel–Trenaunay–Weber syndrome, including “port-wine stains,” varicose veins, hypertrophy of lower extremities, and arteriovenous fistula, as well as an unfortunate development of hypersplenism and nephrotic syndrome. This case report described considerable atypical relevance of Klippel–Trenaunay–Weber syndrome and hypersplenism together with nephrotic syndrome. A multidisciplinary approach was made. Unfortunately, hypersplenism is characterized by pancytopenia that suggests splenectomy, whereas nephrotic syndrome is an indication for renal biopsy; the splenectomy and renal biopsy were delayed due to our patient’s severe condition. Deeper analysis including study of other patients with Klippel–Trenaunay–Weber syndrome would help us to understand the connection between elevated spleen and liver sizes, nephrotic syndrome, and Klippel–Trenaunay–Weber syndrome.

Chemokines and their receptors direct migration and infiltration of immune cells. CCR1 and CCR2 maintain sequence similarity and respond to a number of the same chemokines secreted in lymphoid organs. Expression of CD38 on leukemic cells has been associated with poor clinical outcomes in patients with chronic lymphocytic leukemia (CLL) and is considered as the negative predictor of progression. In our study of newly diagnosed CLL patients, which included 39 CD38-positive and 22 CD38-negative patients, CCR1 and/or CCR2 were always detected, using flow cytometry, on the peripheral blood (PB) CD19⁺CD5⁺ lymphocytes in patients with >30% of the CD38⁺ CD19⁺CD5⁺ lymphocytes (n = 16). Spearman’s rank correlation analysis determined correlations between the frequency of the CCR1- and CCR2-expressing PB CD19⁺CD5⁺ lymphocytes and the frequency of the CD38-positive CD19⁺CD5⁺ lymphocytes (r_s = 0.50 and r_s = 0.38, respectively). No significant correlations were observed between ZAP70 mRNA expression levels in PB mononuclear cells and the frequency of the circulating CCR1⁺ or CCR2⁺ CD19⁺CD5⁺ lymphocytes. Further association studies are needed to verify prognostic relevance of the CCR1/CCR2 expression on leukemic cells in CLL patients at diagnosis. We suggest that CCR1/CCR2 signaling pathways could represent attractive targets for development of CLL anti-progression therapeutics.

We present a rare case of intracranial solitary plasmacytoma arising in brain parenchyma in the basal nuclei. Clinical management and autopsy results of the case are described. Background: Intracranial plasmacytomas arising from brain parenchyma are extremely rare, and data from the literature are limited. Primary intracranial plasmacytomas are rare because plasma cells are not found in the brain in normal conditions. Commonly, intracranial plasmacytoma is associated with multiple myeloma, which is why multiple myeloma must be ruled out to diagnose solitary intracranial plasmacytoma. Considering that solitary plasmacytoma and multiple myeloma have some histopathological similarities, it is important to differentiate them because their respective treatments and prognoses are different. Imaging features of primary extramedullary plasmacytoma are nonspecific but are compatible with solid tumors with invariable enhancement. Plasmacytoma was aggressive because it was not diagnosed after the first MRI, but 1.5 months later, MRI showed a large object. We present a rare case of intracranial solitary plasmacytoma arising in brain parenchyma in the basal nuclei.

Chronic lymphocytic leukemia (CLL) is associated with immune dysfunction, but how disease-intrinsic mechanisms in treatment-naive patients influence the coordination of adaptive responses to novel antigens remains unclear. Here, we assessed SARS-CoV-2-specific antibody and T cell immunity in 38 treatment-naive CLL patients and 13 healthy controls (HCs) following vaccination. Despite significantly reduced total immunoglobulin levels compared to HCs, 94.7% of CLL patients developed SARS-CoV-2-specific IgG, and 89.5% mounted IgA responses, with serum titers comparable to those of HCs. Virus-specific T cell responses, measured by IFN-γ release following antigen stimulation, were detected in 78.9% of patients. CLL patients had significantly more circulating CD4⁺ T follicular helper (Tfh) and T follicular regulatory (Tfr) cells than HCs. These expansions correlated with B cell abundance, which, in untreated CLL, predominantly reflects malignant B cells. Notably, Tfh cell frequencies and absolute counts were highest in patients lacking a SARS-CoV-2-specific T cell response, indicating a decoupling between Tfh expansion and functional antiviral immunity. Overall, these findings demonstrate that while SARS-CoV-2-specific immune responses are largely preserved in treatment-naive CLL patients, disease-driven alterations in T cell composition may compromise the coordination and quality of antigen-specific T cell-mediated immunity.