Influencing factors of lung cancer in nonsmoking women: systematic review and meta-analysis.

BACKGROUND: Epidemiological studies have shown that some factors other than smoking may affect the risk of lung cancer in women, but the results are controversial. We conducted a meta-analysis to summarize the influencing factors of lung cancer in nonsmoking women. METHODS: Both English and Chinese databases were searched for publications from 1990 to 2020. All included studies were assessed according to the Newcastle-Ottawa Scale (NOS). The pooled odds ratios (ORs) and 95% confidence interval (CI) of influential factors were analyzed using the meta-analysis method, and the publication bias and sensitivity were analyzed. RESULTS: Among the five categories, the pooled OR of cooking factors category was the highest. Among 42 influencing factors, there were frequent fried food (OR = 2.42, 95% CI: 1.73-3.38) and long menstrual cycle (0.54, 95% CI: 0.39-0.75). A positive association of history of lung diseases/family lung/all cancer with lung cancer among Asian nonsmoking women (1.82, 95% CI: 1.60-2.07). Unlike other regions, cooking factors were the main risk factor for lung cancer in Asian. CONCLUSION: The meta-analysis suggests that cooking habits, diet, passive smoking, history of cancer and lung disease, and female reproduction are related to lung cancer in nonsmoking women. However, additional studies are warranted to extend this finding.

Cutting edge: influence of the TCR V beta domain on the avidity of CD1d:alpha-galactosylceramide binding by invariant V alpha 14 NKT cells.

CD1d tetramers loaded with alpha-galactosylceramide (alpha-GalCer) bind selectively to mouse invariant Valpha14 (Valpha14i) NKT cells and their human counterparts. Whereas tetramer binding strictly depends on the expression of a Valpha14-Jalpha18 chain in murine NKT cells, the associated beta-chain (typically expressing Vbeta8.2 or Vbeta7) appears not to influence tetramer binding. In this study, we describe novel alpha-GalCer-loaded mouse and human CD1d-IgG1 dimers, which revealed an unexpected influence of the TCR-beta chain on the avidity of CD1d:alpha-GalCer binding. A subset of Valpha14i NKT cells clearly discriminated alpha-GalCer bound to mouse or human CD1d on the basis of avidity differences conferred by the Vbeta domain of the TCR-beta chain, with Vbeta8.2 conferring higher avidity binding than Vbeta7.

Encephalitogenic activity of truncated myelin oligodendrocyte glycoprotein (MOG) peptides and their recognition by CD8+ MOG-specific T cells on oligomeric MHC class I molecules.

We have previously demonstrated that the 21-residue peptide pMOG(35-55) from myelin oligodendrocyte glycoprotein (MOG) contains an antigenic epitope that activates CD8(+) encephalitogenic T cells in C57BL/6 (B6) mice. To identify the core encephalitogenic epitope of CD8(+) MOG-specific T cells, we have prepared a panel of highly purified peptides of varying lengths, which span the entire length of pMOG(35-55), and tested their binding to recombinant H-2D(b) dimers and their ability to induce EAE. Two of the truncated peptides, pMOG(40-54) and pMOG(44-54), strongly bound recombinant H-2D(b) protein and this complex bound MOG-specific CD8(+) T cells. Interestingly, pMOG(40-54) retained the full capability of inducing paralytic disease, whereas only a part of the B6 mice immunized with pMOG(44-54) developed clinical paralysis and central nervous system (CNS) inflammation. Further deletion of 1 amino acid from either the N- or C-terminus of the peptide pMOG(44-54) dramatically reduced binding to recombinant H-2D(b), and abolished the induction of paralysis and CNS inflammation. Our results demonstrate that the ability of truncated pMOG(35-55) peptides to bind recombinant H-2D(b) protein does not always correlate with their ability of inducing encephalomyelitis. This approach enables the further identification of the core pathogenic epitope within the pMOG(35-55) that activates MOG-specific encephalitogenic CD8(+) T cells.