PubMed · 7796726
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J Steurer, U Hoffmann, W Vetter. 1995-06-16. [The hyperventilation syndrome].. https://doi.org/10.1055/s-2008-1055422
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Cytotoxic T lymphocyte (CTL or CD8) responses are a major branch of the immune system involved in controlling viral infections. Murine models have shown that the development of effective and sustained CD8 cell responses requires CD4 T cell help. However, the precise mechanism in which CD4 cells provide help for CD8 cell responses is still controversial. In the literature, mainly two mechanisms are discussed. According to the "classical" pathway, CD4 cells secrete cytokines, such as IL-2, which promote the responsiveness of the CD8 cells. According to the "CD4-APC-CD8" pathway, CD4 cells specifically activate antigen presenting cells (APCs), and APCs specifically interact with CD8 cells, thereby delivering help. Here, we derive kinetic models in order to describe and compare both pathways of help. We find that the two pathways might have different roles in different situations. The classical pathway is more efficient at inducing CD8 cell expansion at high virus loads, while the CD4-APC-CD8 pathway is more efficient at inducing CD8 cell proliferation at low virus loads. From this, it follows that the classical pathway might be needed in order to kick-start a CD8 cell response in the acute phase of the infection, while the CD4-APC-CD8 pathway is needed in order to ensure virus clearance when virus load is reduced by the immune system. These findings have implications for the interpretation of experimental data from virus infection in helper-deficient hosts. In particular, the models offer further suggestions for the development of treatment regimes aimed at achieving immunological control of HIV infection which has been shown to crucially depend on the availability of helper cell responses.
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Previous studies have shown higher levels of Chlamydia pneumoniae (C. pneumoniae, CP) antibody titers (CPIgG), C-reactive protein (CRP), and fibrinogen in patients with coronary artery disease. The role of these infectious and inflammatory markers in precipitating acute coronary syndrome (ACS) is unclear. We conducted a cross-sectional study on patients (n = 830, mean age 63 +/- 15 years, 57% male) admitted to the chest pain center of our institution. The differences in the CPIgG, CRP, and fibrinogen levels in patients who were diagnosed with ACS versus those who were not (non-ACS) were evaluated. CPIgG titers tended to be higher in the ACS group than in the non-ACS group. However, when different titers were used to define seropositivity, the difference achieved statistical significance only at the titer of > or =1:1,024 (35% vs 26%, p = 0.004). CRP (median 0.48 vs 0.33 mg/dl, p <0.0001), fibrinogen (median 317 vs 293 mg/dl, p <0.0001), and leukocyte count (median 7.7 vs 6.9 10(9)/L, p <0.0001) were higher in the ACS group. On multivariate analysis, CPIgG > or =1:1,024 (odds ratio [OR] 1.62), diabetes (OR 1.91), hypertension (OR 1.46), prior myocardial infarction (OR 1.78), smoking (OR 1.70), Caucasian race (OR 1.7), high-density lipoprotein (OR 0.98), and elevated troponin-T (OR 12.44) were the only factors independently associated with ACS. Thus, we found a strong association between high level seropositivity to CP and ACS. This may indicate recent re-infection or an exaggerated immune response to CP as an etiologic factor for ACS. This study also suggests that therapeutic interventions may need to be specifically targeted to these patients.