The impact of weather on mental illness is widely debated, but the mechanism of this relationship remains unclear. The immunoseasonal theory suggests that in winter, a T-helper 1 (Th1) response predominates, impairing Prefrontal Cortex (PFC) control, which exacerbates symptoms of depression, while after it, in summer, a Th2 response predominates in immunologically prone individuals, activating cortical and mesolimbic centers, which can exacerbate symptoms of psychosis. In this paper, we aim to describe the validity of this theory through a narrative review of data related to weather and immunology in psychiatry. This review extends existing literature by integrating immunological findings with psychiatric seasonality research, offering a mechanistic perspective that links Th1/Th2 shifts to specific symptom exacerbations. Winter Th1 severity may worsen depression and anxiety, while summer Th2 dominance appears to be associated with exacerbations of schizophrenia, mania, impulsivity, and suicide risk. It is possible that the mechanism of Th1 response potentiation and deterioration of PFC function is common to most psychiatric entities and is nonspecific. This suggests that seasonal immune dysregulation may play a broader role in psychiatric disorders than previously recognized, challenging the idea that seasonality impacts only selected conditions. Characteristic dysfunctions within an individual determine further differences in clinical manifestations. The mechanism of Th2 potentiation may not be limited to mania and psychosis but may also be associated with increased impulsivity and suicide risk. If the immunoseasonal theory is confirmed, selected immunological markers could be used not only in the diagnosis of psychiatric exacerbations but also in predicting symptom fluctuations and tailoring treatment strategies. This could enable more personalized interventions, such as seasonally adjusted medication dosing or targeted anti-inflammatory therapies. While this mechanism seems plausible, further research, especially analyzing markers of inflammatory and anti-inflammatory responses, is needed to better understand and confirm it.

Necrobiosis lipoidica (NL) is a rare granulomatous disease of a not fully understood etiopathogenesis. Classically, NL is associated with insulin-dependent diabetes mellitus. The disease often fails to respond to conventional treatments and adversely affects patients’ quality of life. First-line medications are usually topical corticosteroids, but patients respond to them with varying degrees of success. Other options include tacrolimus, phototherapy, cyclosporine, fumaric acid esters, and biologics (adalimumab, etanercept, and infliximab). Our review aims to present new therapeutic approaches potentially effective in patients with refractory lesions, describe the presumed etiopathogenesis, and provide diagnostic guidance for clinicians. The review concludes that Janus kinase inhibitors and biologics such as ustekinumab and secukinumab can be used effectively in patients with recalcitrant NL. Another promising treatment option is tapinarof (an aryl hydrocarbon receptor agonist). However, studies on larger groups of patients are still needed to evaluate the effectiveness of different therapeutic options and to define consistent treatment regimens for NL. It is advisable to improve the awareness of physicians of various specialties regarding necrobiosis lipoidica as lesions diagnosed earlier usually have a better response to treatment.

Numerous scientific findings indicate that excess adipose tissue, particularly visceral fat, is associated with a chronic inflammatory state manifested by elevated levels of proinflammatory cytokines and an imbalance in the T helper type 1/type 2 (Th1/Th2) response, which carries numerous metabolic consequences. Obesity induces, among other effects, the activation of the kynurenine pathway and a reduction in serotonin synthesis, alterations in adipokine profiles, modifications of the hypothalamic–pituitary–adrenal (HPA) axis, disturbances in fatty acid ratios, oxidative stress, and dysfunction of the gamma-aminobutyric acid (GABA)ergic system. These neuroimmunological and metabolic disturbances, along with obesity-induced neurotransmission abnormalities that may represent a common underlying model of depression, could provide valuable insights into the pathomechanisms of depression, allowing for prediction of disease progression and individualized therapeutic strategies in overweight patients. Furthermore, the analysis of inflammation-associated biomarkers opens up new therapeutic perspectives, suggesting that interventions aimed at reducing inflammation might lead to potential advances in the treatment of depression.

Emerging evidence highlights the role of chronic low-grade inflammation and dysregulated cytokines in both obesity and schizophrenia, suggesting overlapping immune system pathways that contribute to cognition and nervous system inflammation. Excess adipose tissue functions as an active endocrine organ, releasing pro-inflammatory mediators that may serve as potential biomarkers, while the use of antipsychotic agents in schizophrenia further modifies cytokine profiles and immune responses. A key knowledge gap lies in understanding how adipose-related inflammation modifies the severity of psychotic symptoms, cognitive deficits, and the efficacy of antipsychotic medications. This review aims to present excess adipose tissue as a potential contributor to the development of SCZ or a modifier of treatment efficacy, emphasizing the role of immune imbalance, inflammatory pathways, and metabolic dysfunction. By synthesizing current findings, we aim to present obesity not only as a frequent comorbidity in schizophrenia but also as a potential driver of neuroinflammation and disease progression. Here, we demonstrate that excess adiposity may perpetuate a vicious cycle linking metabolic dysfunction, immune activation, and psychiatric symptomatology. Situating these findings within a broader context, the review underscores the clinical need for inflammation-informed, individualized management strategies that integrate psychiatric care with metabolic monitoring. Ultimately, clarifying the shared inflammatory pathways of obesity and schizophrenia may open new avenues for biomarker development and targeted interventions.

With the increased availability of hybrid PET/MRI in recent years, this method is increasingly used for neuroimaging in clinical practice. It combines the advantages of MRI (including high-resolution imaging of intracerebral lesions and data provided from specialised MRI sequences) with the benefits of PET, which visualises functional alterations in the brain, as well as assesses the myelin quantity changes and the severity of inflammation. The use of PET/MRI may help to eliminate the limitations of MRI indicated in imaging demyelinating inflammatory diseases (such as low specificity in imaging demyelination and a weak correlation of findings with clinical symptoms), as well as insufficient sensitivity in detecting lesions present in encephalitis. In addition to supporting the diagnosis of encephalitis, PET/MRI facilitates monitoring of the disease course and assessing the treatment efficacy of inflammatory demyelinating diseases and encephalitis, as well as evaluating the risk of multiple sclerosis relapse. Further multi-centre longitudinal studies are necessary to assess the real clinical potential of PET/MRI among patients with inflammatory demyelination or encephalitis. In addition to MS and AIE, these studies should also include other inflammatory demyelinating diseases (ADEM, NMO, NMOSD, and MOGAD) as well as encephalitis of viral and parasitic aetiology.

The impact of weather on mental illness is widely debated, but the mechanism of this relationship remains unclear. The immunoseasonal theory suggests that in winter, a T-helper 1 (Th1) response predominates, impairing Prefrontal Cortex (PFC) control, which exacerbates symptoms of depression, while after it, in summer, a Th2 response predominates in immunologically prone indyviduals, activating cortical and mesolimbic centers, which can exacerbate symptoms of psychosis. This paper discusses the evidence for the immuneseasonal theory, with a particular focus on the inflammatory profile in psychiatry and seasonal exacerbations of mental illness. Winter Th1 severity may worsen depression and anxiety, while summer Th2 dominance appears to be associated with exacerbations of schizophrenia, mania, impulsivity, and suicide risk. It is possible that the mechanism of Th1 response potentiation and deterioration of PFC function is common to most psychiatric entities and is nonspecific. Characteristic dysfunctions within an individual determine further differences in clinical manifestations. The mechanism of Th2 potentiation may not be limited to mania and psychosis, but may also be associated with increased impulsivity and suicide risk. While this mechanism seems plausible, further research, especially analyzing markers of inflammatory and anti-inflammatory responses, is needed to better understand and confirm it.