RESUMO
Multiple sclerosis (MS) is a life-threading disease that poses a great threat to the human being lifestyle. Having said extensive research in the realm of underlying mechanisms and treatment procedures, no definite remedy has been found. Over the past decades, many medicines have been disclosed to alleviate the symptoms and marking of MS. Meanwhile, the substantial efficacy of herbal medicines including curcumin must be underscored. Accumulated documents demonstrated the fundamental role of curcumin in the induction of the various signaling pathways. According to evidence, curcumin can play a role in mitochondrial dysfunction and apoptosis, autophagy, and mitophagy. Also, by targeting the signaling pathways AMPK, PGC-1α/PPARγ, and PI3K/Akt/mTOR, curcumin interferes with the metabolism of MS. The anti-inflammatory, antioxidant, and immune regulatory effects of this herbal compound are involved in its effectiveness against MS. Thus, the present review indicates the molecular and metabolic pathways associated with curcumin's various pharmacological actions on MS, as well as setting into context the many investigations that have noted curcumin-mediated regulatory effects in MS.
RESUMO
Innate lymphoid cells (ILCs) as key players in innate immunity have been shown to be significantly associated with inflammation, lymphoid neogenesis, tissue remodeling, mucosal immunity and lately have been considered a remarkable nominee for either tumor-promoting or tumor-inhibiting functions. This dual role of ILCs, which is driven by intrinsic and extrinsic factors like plasticity of ILCs and the tumor microenvironment, respectively, has aroused interest in ILCs subsets in past decade. So far, numerous studies in the cancer field have revealed ILCs to be key players in the initiation, progression and inhibition of tumors, therefore providing valuable insights into therapeutic approaches to utilize the immune system against cancer. Herein, the most recent achievements regarding ILCs subsets including new classifications, their transcription factors, markers, cytokine release and mechanisms that led to either progression or inhibition of many tumors have been evaluated. Additionally, the available data regarding ILCs in most prevalent cancers and new therapeutic approaches are summarized.
Assuntos
Imunidade Inata , Linfócitos/imunologia , Neoplasias/imunologia , Microambiente Tumoral , Animais , Biomarcadores , Transformação Celular Neoplásica , Citocinas/metabolismo , Progressão da Doença , Humanos , Imunoterapia , Inflamação/imunologia , Linfócitos/patologia , Neoplasias/metabolismo , Resultado do TratamentoRESUMO
Innate lymphoid cells (ILCs) are kind of innate immune cells which can be divided into three main subsets according to their cytokine release profile, transcription factors, and surface markers. ILCs affect the initial stages of immunity in response to microbes and participate in immunity, inflammation, and tissue repair. ILCs modulate immunity through resistance to the pathogens and regulation of autoimmune inflammation and metabolic homeostasis. Therefore dysregulation of ILCs may lead to chronic pathologies such as allergies (i.e., asthma), inflammation (i.e., inflammatory bowel disease), and autoimmunity (i.e., psoriasis, atopic dermatitis, rheumatoid arthritis, multiple sclerosis, and ankylosing spondylitis). Regarding the critical role of ILCs in the regulation of immune system, the elucidation of their function in different conditions makes an interesting target for improvement of novel therapeutic approach to modulate an immune response in different disease context.
Assuntos
Doenças Autoimunes/imunologia , Hipersensibilidade/imunologia , Imunidade Inata , Inflamação/imunologia , Linfócitos/imunologia , Animais , Doenças Autoimunes/metabolismo , Citocinas/imunologia , Citocinas/metabolismo , Humanos , Hipersensibilidade/metabolismo , Inflamação/metabolismo , Mediadores da Inflamação/imunologia , Mediadores da Inflamação/metabolismo , Linfócitos/metabolismo , Fenótipo , Transdução de SinaisRESUMO
Programmed cell death-ligand 1 (PD-L1) is a glycoprotein that is expressed on the cell surface of both hematopoietic and nonhematopoietic cells. PD-L1 play a role in the immune tolerance and protect self-tissues from immune system attack. Dysfunction of this molecule has been highlighted in the pathogenesis of tumors, autoimmunity, and infectious disorders. MicroRNAs (miRNAs) are endogenous molecules that are classified as small non-coding RNA with approximately 20-22 nucleotides (nt) length. The function of miRNAs is based on complementary interactions with target mRNA via matching completely or incompletely. The result of this function is decay of the target mRNA or preventing mRNA translation. In the past decades, several miRNAs have been discovered which play an important role in the regulation of PD-L1 in various malignancies. In this review, we discuss the effect of miRNAs on PD-L1 expression and consider the effect of miRNAs on the synthetic pathway of PD-L1, especially during cancers.