Histopathological Correlation in Different Types of Leprosy in a Tertiary Health Care Centre

Hansen’s disease or Leprosy, is a chronic infectious disease that is contagious and has a slow evolution. It affects mainly skin and schwann cells in the peripheral nerves and causes peripheral neuropathy which contributes to the permanent functional impairments [1]. It is caused by a rod shaped,acid fast staining bacteria known as Mycobacterium Leprae which has parallel sides, round ends and a characteristic bundle of cigar appearance due to the presence of a glial substance which is a surface lipid that makes the bacilli to be arranged side by side in parallel arrays [2]. It has a distinctive empathy towards the peripheral nerves where it establishes originally therefore it is the site where the pathological processes start mainly with the principal target being Schwann cell [3,4]. Amidst the communicable diseases, Leprosy is the most common cause of physical disabilities which is permanent. When the bacterium enters a person with good cell-mediated immunity against it, it gets destroyed. If there is a slight impairment in the cell-mediated immunity against it, some bacilli will multiply and a lesion develops. Depending upon the immune status of a host, it expresses itself in different clinico-histopathological forms [5]. Ridley and Jopling suggested a five-group classification of leprosy known as immunological classification based upon the immunological status of the patient as (a) tuberculoid (TT), (b) borderline tuberculoid (BT), (c) mid-borderline (BB), (d) borderline lepromatous (BL) and (e) lepromatous (LL) [6]. Bacteriological, immunological, clinical and histopathological features exhibit continuous but slow changes from one pole to another pole. The main disadvantage of this classification is that there is no specific position for pure neuritic as well as indeterminate leprosy in the spectrum [7].

Tumor Immune Microenvironment and Immunosuppressive Therapy in Hepatocellular Carcinoma: A Review

Liver cancer has the fourth highest mortality rate of all cancers worldwide, with hepatocellular carcinoma (HCC) being the most prevalent subtype. Despite great advances in systemic therapy, such as molecular-targeted agents, HCC has one of the worst prognoses due to drug resistance and frequent recurrence and metastasis. Recently, new therapeutic strategies such as cancer immunosuppressive therapy have prolonged patients’ lives, and the combination of an immune checkpoint inhibitor (ICI) and VEGF inhibitor is now positioned as the first-line therapy for advanced HCC. Since the efficacy of ICIs depends on the tumor immune microenvironment, it is necessary to elucidate the immune environment of HCC to select appropriate ICIs. In this review, we summarize the findings on the immune microenvironment and immunosuppressive approaches focused on monoclonal antibodies against cytotoxic T lymphocyte-associated protein 4 and programmed cell death protein 1 for HCC. We also describe ongoing treatment modalities, including adoptive cell transfer-based therapies and future areas of exploration based on recent literature. The results of pre-clinical studies using immunological classification and animal models will contribute to the development of biomarkers that predict the efficacy of immunosuppressive therapy and aid in the selection of appropriate strategies for HCC treatment.

Immunological classification of gliomas based on immunogenomic profiling

Background Gliomas are heterogeneous in the tumor immune microenvironment (TIM). However, a classification of gliomas based on immunogenomic profiling remains lacking. Methods We hierarchically clustered gliomas based on the enrichment levels of 28 immune cells in the TIM in five datasets and obtained three clusters: immunity-high, immunity-medium, and immunity-low. Results Glioblastomas were mainly distributed in immunity-high and immunity-medium, while lower-grade gliomas were distributed in all the three subtypes and predominated in immunity-low. Immunity-low displayed a better survival than other subtypes, indicating a negative correlation between immune infiltration and survival prognosis in gliomas. IDH mutations had a negative correlation with glioma immunity. Immunity-high had higher tumor stemness and epithelial-mesenchymal transition scores and included more high-grade tumors than immunity-low, suggesting that elevated immunity is associated with tumor progression in gliomas. Immunity-high had higher tumor mutation burden and more frequent somatic copy number alterations, suggesting a positive association between tumor immunity and genomic instability in gliomas. Conclusions The identification of immune-specific glioma subtypes has potential clinical implications for the immunotherapy of gliomas.