Review Article
Yahya Ehteshaminia; Forough Golsaz-Shirazi; Mohammad Mehdi Amiri; Fazel Shokri
Abstract
Pertussis is a highly contagious respiratory disease caused by the gram-negative bacterium Bordetella pertussis (Bp). The disease is most severe in infants and young children, whereas adolescents and adults typically experience milder symptoms but serve as important reservoirs for transmission. Despite ...
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Pertussis is a highly contagious respiratory disease caused by the gram-negative bacterium Bordetella pertussis (Bp). The disease is most severe in infants and young children, whereas adolescents and adults typically experience milder symptoms but serve as important reservoirs for transmission. Despite widespread vaccination efforts, pertussis continues to pose a significant public health challenge. Historically, the first generation of pertussis vaccines, formulated as inactivated whole cell pertussis (wP) vaccines, were associated with notable side effects, prompting the development of safer acellular pertussis (aP) vaccines. The second generation of pertussis vaccines contains purified components of Bp and provides protection comparable to that of the older whole-cell vaccines. However, recent studies have reported a resurgence of pertussis, attributed to several factors, including improved diagnostic methods, waning immunity following vaccinations, and the emergence of antigenically divergent or vaccine-adapted strains. To address these challenges, researchers are developing next-generation pertussis vaccines using various approaches, such as transitioning from intramuscular to intranasal administration, formulating outer membrane vesicle (OMV)-based vaccines, designing live attenuated pertussis vaccines, and exploring nucleic acid-based vaccines and novel adjuvants aimed at inducing long-lasting mucosal and systemic immunity. This review primarily focuses on assessing the efficacy of the next-generation intranasally administered pertussis vaccines in both pre-clinical and clinical settings.
Review Article
Yuan Xia; Jing Niu; Hengheng Fan; Lin Liu; Yuan Zhou; Yuyun Xiong; Yumei Li
Abstract
Keloid, as a skin fibrotic proliferative disorder, have a complex pathogenesis that remains incompletely understood. It is characterized by abnormal and excessive scar formation following skin injury. The occurrence and development of keloids are closely associated with immune dysregulation. Immune cells, ...
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Keloid, as a skin fibrotic proliferative disorder, have a complex pathogenesis that remains incompletely understood. It is characterized by abnormal and excessive scar formation following skin injury. The occurrence and development of keloids are closely associated with immune dysregulation. Immune cells, such as T cells, macrophages, mast cells, and Langerhans cells, play crucial roles in the formation of keloids. These immune cells contribute to keloid initiation and progression through mechanisms including cytokine secretion, promotion of inflammatory responses, and regulation of fibroblast proliferation and collagen synthesis. With advances in immunological research, the roles of fibroblasts, keratinocytes and melanocytes in the immunological dysregulation underlying keloids have received increasing attention. This paper aims to review recent progress on the abnormal immunological regulation involving these three epidermal cell types, in order to provide new insights and theoretical foundations for the treatment of this disease.
Letter To The Editor
Mohammad Hasan Soheilifar; Hoda Keshmiri Neghab; Sima Nobari
Abstract
Wound healing is a complex and dynamic process that encompasses four interrelated phases: hemostasis, inflammation, proliferation, and remodeling. Inflammation plays a pivotal role in both acute and chronic wound healing. In chronic diabetic wounds, the normal healing rate is impaired due to persistent ...
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Wound healing is a complex and dynamic process that encompasses four interrelated phases: hemostasis, inflammation, proliferation, and remodeling. Inflammation plays a pivotal role in both acute and chronic wound healing. In chronic diabetic wounds, the normal healing rate is impaired due to persistent inflammation, which is associated with unbalanced immune responses. Microbial biofilms, increased immune cell activity, the accumulation of pro-inflammatory cytokines, and free radicals can contribute to the establishment of chronic inflammation in these wounds. Modulating the immune microenvironment in chronic wounds can significantly enhance the process of wound healing and tissue regeneration. Programmed death-ligand 1 (PD-L1) is an important immune checkpoint molecule that can bind to the PD-1 receptor on the immune cells and suppress the immunogenic responses. Although inflammation plays a significant role in wound healing, the role of PD-L1 in chronic wounds is not clearly understood. Interestingly, recent evidence indicates that fibroblast cells in granulation tissues express PD-L1. This paper will review the current findings and potential advantages of PD-L1 in the wound healing process, presenting a novel approach for treating chronic wounds.
Original Article
Eida Elmansorry
Abstract
Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and progressive destruction of joint structures. Anti-cyclic citrullinated peptide (anti-CCP) antibodies have emerged as highly specific biomarkers, whereas rheumatoid factor (RF) demonstrates ...
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Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and progressive destruction of joint structures. Anti-cyclic citrullinated peptide (anti-CCP) antibodies have emerged as highly specific biomarkers, whereas rheumatoid factor (RF) demonstrates lower diagnostic specificity.
Objective: To assess the diagnostic utility of anti-CCP in comparison with rheumatoid factor (RF) in Libyan patients with RA and to investigate their associations with immunological markers, demographic characteristics, comorbid conditions , and clinical manifestations.
Methods: A cross-sectional case-control study was conducted involving70 RA patients who met the 2010 ACR/EULAR classification criteria and 70 age- and sex-matched healthy controls. Serum concentrations of anti-CCP antibodies, RF, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and complete blood count parameters were measured. Statistical analyses were performed to evaluate associations between serological markers and clinical variables, including sex, age, family history, disease activity, comorbidities, smoking status, COVID-19 vaccination, and vitamin D levels.
Results: Anti-CCP demonstrated a higher positivity rate (78.6%) compared with RF (64.3%) and was negative in all controls, whereas RF yielded false-positive results. Anti-CCP positivity was significantly associated with female sex (p = 0.026), tender joint count, CRP, ESR, neutrophil-to-lymphocyte ratio, platelet count, and mean corpuscular volume. Additional associations were identified with COVID-19 vaccination, smoking, type 1 diabetes mellitus, family history of RA, higher disease activity, and lower vitamin D levels.
Conclusion: Anti-CCP demonstrated superior diagnostic specificity and broader clinical relevance compared with RF. Its strong associations with female sex, family history of RA, comorbidities, and disease activity support the incorporation of anti-CCP testing into routine diagnostic and monitoring protocols for RA in Libya.
Original Article
Zahra Mansourabadi; Ali Moazzeni; Majid Akrami; Maryam Fakhimi; Zahra Faghih
Abstract
Background: Tumor-draining lymph nodes play a pivotal role in orchestrating immune cell trafficking and initiating antitumor responses. Among immunoregulatory molecules, programmed cell death protein 1 (PD-1) has emerged as a central mediator in tumor-induced immunosuppression.
Objective: To investigate ...
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Background: Tumor-draining lymph nodes play a pivotal role in orchestrating immune cell trafficking and initiating antitumor responses. Among immunoregulatory molecules, programmed cell death protein 1 (PD-1) has emerged as a central mediator in tumor-induced immunosuppression.
Objective: To investigate the expression patterns of PD-1 and its ligands (PD-L1, PD-L2) in the tumor-draining lymph nodes of patients with breast cancer (BC).
Methods: Lymph node samples were freshly collected from BC patients undergoing surgery. Mononuclear cells were isolated and analyzed by flow cytometry for surface markers CD45, PD-1, PD-L1, and PD-L2. Data were analyzed using FlowJo v10.8.1.
Result: PD-1 was detected on 9.48 ± 5.19% of CD45+ cells, whereas PD-L1 and PD-L2 were expressed at lower levels (1.73 ± 0.85% and 1.68 ± 0.84%, respectively). Despite a significant reduction in the percentage of CD45+ lymphocytes, the frequencies of PD-1+ and PD-L2+ subsets were significantly elevated in patients with poorly-differentiated and advanced-stage tumors (P<0.05). Additionally, the frequency of PD-1+ lymphocytes was significantly higher in patients with the triple-negative tumors (P=0.014) and in those negative for estrogen and progesterone receptor (P=0.001).
Conclusion: Elevated expression of PD-1 and its ligands in BC-draining lymph nodes is associated with adverse clinical features, suggesting their role in immune evasion. These findings along with higher frequency of PD-1+ lymphocyte in triple-negative patients may inform subtype-specific therapeutic strategies and predict responsiveness to PD-1/PD-Ls blockade therapies. Future studies should include functional analyses with broader immunophenotyping to further elucidate these mechanisms.
Original Article
Chenxi Li; Mingxin Lin; Min Zhu; Jianmin Lin; Xiujuan Li; Huiming Ye
Abstract
Background: Proper invasion and migration of trophoblasts are critical for successful human pregnancy. Tumor necrosis factor-α (TNF-α) has two biologically active forms: the membrane-bound TNF-α (mTNF) and the soluble TNF-α (sTNF).
Objective: To investigate the role of both forms ...
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Background: Proper invasion and migration of trophoblasts are critical for successful human pregnancy. Tumor necrosis factor-α (TNF-α) has two biologically active forms: the membrane-bound TNF-α (mTNF) and the soluble TNF-α (sTNF).
Objective: To investigate the role of both forms of TNF-α in trophoblasts invasion and migration and to elucidate their underlying mechanisms.
Methods: We exposed HTR-8/SVneo trophoblasts to exogenous mTNF or sTNF and evaluated their cellular behaviors. Proliferation was assessed using a Cell Counting Kit-8, while invasion and migration were assessed through Transwell assays. Additionally, we measured mRNA levels of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinases-1 (TIMP-1), and plasminogen activator inhibitor-1 (PAI-1) using qRT-PCR. The expression of IκB-α was determined by western blot analysis.
Results: Unlike sTNF, mTNF enhances the invasion and migration of trophoblasts. Mechanistic analysis showed that mTNF increased MMP-9 expression while decreasing TIMP-1 and PAI-1 expression, and it inhibited the activation of NF-κB signaling pathway in HTR-8/SVneo cells with or without lipopolysaccharide (LPS) treatment.
Conclusion: This research uncovered a new function of mTNF in regulating trophoblast invasion and migration, offering a new approach to treating pregnancy-related diseases associated with inadequate trophoblast invasion.
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