BackgroundRheumatoid meningitis (RM) is a rare disorder that often develops during a remission phase of rheumatoid arthritis (RA). This is the first study to demonstrate differences in regard to immunological disturbance between blood and cerebrospinal fluid (CSF) samples obtained from a patient with RM using flow cytometry.Case presentationA 36-year-old woman with RA and generalized myasthenia gravis (MG) developed RM during a remission phase. Although both RA and MG were stable and well controlled, she noticed fever, headache, and transient sensory disturbance. Blood and CSF examination findings suggested aseptic meningitis, while brain magnetic resonance imaging revealed restricted portions of meningitis and associated cortical lesions, compatible with a diagnosis of RM. The dose of oral prednisolone was increased, which ameliorated the symptoms within 1 week along with improvement in CSF findings. This patient exhibited features of RM that were manifested in a manner independent of the activity of RA. An investigation of cellular immunity using CSF specimens with flow cytometry showed differences in regard to the pathogenesis of inflammation in the CSF as compared to outside of the central nervous system. In contrast to results obtained with paired blood samples, CSF cells at the peak stage of RM showed a marked increase in CCR3+ Th2 cells and marked decrease in CD8+ cells, suggesting an immunoregulatory disturbance in the CSF. Those findings indicated a CSF-specific activation of humoral immunity, resulting in augmentation of meningeal inflammation, as shown by excess synthesis of intrathecal IgG and markedly elevated interleukin-6 level. Results of the present detailed investigation of lymphocyte subsets revealed a discrepancy regarding the process of inflammation in this RM patient between CSF and blood samples.ConclusionsRM is not a simple reflection of the immune status of RA, as the pathogenesis seems related to, at least in part, CSF-specific immunological dysregulation.

Objective Systemic inflammation is known to be associated with Alzheimer's disease (AD) advancement. The aim of the present study was to examine the relationships of cognitive function in AD patients with the presence of systemic inflammation and immunological alterations. Methods Eight patients with AD and nine elderly individuals as a control group were enrolled, none of whom had a history of autoimmune diseases or were suffering from an infection. C-reactive protein, interleukin-6 and tumor necrosis factor-a levels in serum were measured, while lymphocyte subsets were also determined using a flow cytometry system. In addition, two of the AD patients received repeated cognitive function and blood testing on an outpatient basis. Results In the AD group, the percentages of CD3 À CD16 + CD56 + (natural killer) and CD4 + CCR5 + (type 1 helper T) cells, and CD8 + CD11a + (cytotoxic T) lymphocytes were increased, whereas the percentages of CD19 + (B lymphocytes) and CD4 + CD25 bright CD127 dim (regulatory T) cells were decreased as compared with the controls. Systemic inflammation, represented by elevated C-reactive protein and interleukin-6, was shown to aggravate cognitive function in both patients who underwent follow-up outpatient examinations. However, lymphocyte subsets did not change in parallel with cognitive function. Conclusions Inflammatory acute clinical events have the potential to reduce cognitive function in AD patients, which could be partially attributed to a decrease in regulatory T cells in the blood. Furthermore, increased numbers of natural killer cells, cytotoxic T lymphocytes and type 1 helper T cells in these patients might reflect the presence of chronic inflammation, thus forming an immunological background.

It is known that mumps is an acute and highly contagious systemic viral infection that occurs in childhood, the hallmark of which is parotid gland swelling. Although mumps infection in the central nervous system (CNS) is uncommon among adults in association with vaccinations generally administered in developed countries, CNS involvement can occur without parotitis. Here, we report such a case of severe meningitis due to reinfection by the mumps virus. Based on our findings, we propose that mumps meningitis can mimic tuberculous meningitis in regard to clinical symptoms and course, as well as laboratory test results of cerebrospinal fluid. Follow-up investigations that include key cytokines such as IL-6, IFN-γ, and TNF-β in the CSF are important for differential diagnosis.

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