Macrophage Migration Inhibitory Factor (MIF) is a pleiotropic cytokine that acts as a central regulator of inflammation and immune responses across diverse organ systems. Functioning upstream in immune activation cascades, MIF influences macrophage polarization, T and B cell differentiation, and cytokine expression through CD74, CXCR2/4/7, and downstream signaling via NF-κB, ERK1/2, and PI3K/AKT pathways. This review provides a comprehensive analysis of MIF’s mechanistic functions under both physiological and pathological conditions, highlighting its dual role as a protective mediator during acute stress and as a pro-inflammatory amplifier in chronic disease. MIF’s involvement in autoimmune disorders, neurodegeneration, metabolic syndromes, infectious diseases, and oncogenesis is examined, with particular attention to its contribution to immune dysregulation, immune escape, and the shaping of inflammatory microenvironments. Its clinical relevance as a biomarker is underscored by associations between elevated serum levels, polymorphic variants such as the -173 G>C SNP, and disease susceptibility, progression, and therapeutic response. Advances in therapeutic strategies are also discussed, including the development of small-molecule inhibitors, MIF-2-specific antagonists, CD74-targeted therapies, and gene-based interventions. Taken together, emerging evidence positions MIF as both a diagnostic indicator and a therapeutic target, with its broad regulatory functions across immune, vascular, and metabolic pathways emphasizing its relevance in precision immunotherapy and its potential to serve as a strategic axis in the future of translational medicine.

Macrophage Migration Inhibitory Factor (MIF) is a key inflammatory cytokine implicated in immune regulation and tumour biology. Its role in lung disease, particularly in relation to tumour differentiation and clinical risk, remains incompletely understood. This study aimed to evaluate the expression pattern of MIF in lung disease using gene expression profiling, assess its variation across histological grades, and determine its association with clinical risk. A secondary data-based exploratory analysis was conducted using microarray gene expression data from 442 lung tissue samples obtained from a publicly available dataset. MIF expression was extracted using probe ID 200799_at from the Affymetrix Human Genome U133A platform. Samples stratified based on histological differentiation into well, moderate, and poorly differentiated groups. Statistical analyses included descriptive statistics, Welch’s t-test, Pearson correlation, and linear regression. MIF expression demonstrated a significant increase with decreasing tumour differentiation, with the highest levels observed in poorly differentiated tumours (11.05±0.68). Independent t-tests confirmed significant differences between all histological groups (p<0.05). However, correlation analysis revealed a weak and non-significant association with clinical risk (r=0.06, p=0.20) and regression analysis indicated minimal predictive power (R²=0.003). MIF expression is significantly associated with tumour differentiation in lung disease but lacks predictive value for clinical risk. These findings suggest that MIF serves as a marker of tumour biology rather than a standalone prognostic biomarker.

Було проведено проспективний мікроскопічний та статистичний аналіз доношених зразків плацентарної тканини та макроскопічних параметрів, отриманих від 20 здорових жінок з неускладненою одноплідною вагітністю (10 чоловічих і 10 жіночих плацент). Для оцінки розмірів плаценти, товщини, ваги, загальної архітектури ворсинок, структури мікросудин та розподілу стромальних клітин було використано звичайну обробку тканин, фарбування гематоксиліном та еозином, а також стандартні описові статистичні оцінки. Описова статистика виявила вихідні фізичні відмінності: середні розміри плаценти становили 21,2±1,3 см для чоловічих плацент і 20,0±1,5 см для жіночих; товщина плаценти становила в середньому 2,50±0,47 см у чоловіків проти 2,52±0,27 см у жінок; а середня вага становила 499,9±45,0 г у групі чоловіків порівняно з 474,6±31,0 г у групі жінок. Гістологічні дослідження виявили зрілу структуру ворсинок в обох групах. Доношені плаценти з цієї групи демонструють незначні морфометричні та мікросудинні відмінності, пов’язані зі статтю плода, зокрема щодо ваги та калібру капілярів.

Oral exposure to lipophilic plant bioactives depends on lipid digestion and enterocyte handling. Long-chain fatty acids and monoacylglycerols can be re-esterified and assembled with apolipoprotein B48 into chylomicrons, creating a route through intestinal lymph that differs from portal delivery. Food-grade lipid nanocarriers may alter this pathway by changing lipid digestion, micellar solubilization, cellular uptake, and chylomicron secretion, yet evidence for lymphatic transport is often inferred from bioaccessibility or plasma exposure rather than measured directly. This review evaluates how triglyceride chain length, unsaturation, lipid physical state, emulsifier interfaces, food matrices, and processing shape the digestive transformation of nanoemulsions and lipid particles into mixed colloids and substrates for enterocyte lipid processing. It compares nanoemulsions, nanostructured lipid carriers, liposomes, and related systems, with attention to the distinction between intact-particle uptake and cargo incorporation into endogenous lipoproteins. Static and dynamic digestion, epithelial models, lymph-duct cannulation, chylomicron-associated analyte measurements, and human pharmacokinetics are considered as distinct evidence tiers. The synthesis identifies which design claims are supported by direct lymph measurements and which remain mechanistic hypotheses. A framework aligns lipid composition and cargo chemistry with the intended portal or lymphatic exposure pathway. By treating endogenous chylomicron assembly as a testable design target, this review distinguishes a route-specific mechanism from gains in solubilization, epithelial uptake, or plasma exposure alone.