TB is typically caused by Mycobacterium tuberculosis, a symbiotic bacterium present in one-third of the world's population. There any many factors triggering overt clinical disease in a small proportion of humans. In our view the major role in the process is played by the host's immune response, especially self-directed, destructive inflammation. Conventional chemotherapy produces bactericidal or bacteriostatic effects, but immunopathological changes can only be corrected by immunotherapy. Various attempts have been made to identify the optimal immune intervention. Some have shown promising effects, but many have failed. It is commonly believed that the field started in 1890: the year Robert Koch announced his tuberculin therapy. In the Pên Ts'ao Kang Mu, classical Chinese materia medica, published during Ming dynasty, Li Shi Chen (1518-1593) recommended, as a remedy for hemoptysis, to collect from the sputum "…blood lumps, roast them till they are black, and take then them as a powder". In retrospect, this is perhaps the earliest recorded reference relating to immunotherapy of TB with heat-killed mycobacteria. Modern science is obviously geared toward more palatable approach, but without hindsight from often disdained empirical evidence no progress can be made. The clinical experience from various trial and error processes is briefly discussed in this review.

The proposed therapeutic regimen enabled complete suppression of residual interferon-α antiviral activity, an increase in interleukin-4 that regulates local humoral immunity, and a decrease (down to a complete suppression) in anti-inflammatory interleukin-2, which is responsible for activation of cell-mediated immunity, thus, resulting in resolution of the immune-mediated inflammation in the cornea.

Blood immunological parameters (cytokine profile and interferon status) and the level of monoamines and their metabolites in various brain structures (amygdala, hippocampus, septum, and hypothalamus) were studied in rats kept under standard conditions or in overpopulated cages. Long-term overcrowding was associated with reduced expression of IL-4 gene, increased transcription of IL-17, and decreased production of IFN-γ, which attested to impaired humoral and cell-mediated immunity and disturbances in IFN-γ synthesis at the post-transcriptional level. Under these conditions, the levels of norepinephrine and dopamine decreased in the septum, but increased in the hypothalamus. The amount of dopamine metabolite dihydroxyphenylacetic acid decreased in both these structures, and the index of dopamine metabolism (dihydroxyphenylacetic acid/dopamine ratio, DOPAC/dopamine) decreased only in the hypothalamus. Overcrowding was not followed by changes in the parameters of noradrenergic and dopaminergic systems in the amygdala and hippocampus and serotoninergic system in all study structures.

Leukoplakia of the oral mucosa is characterized by impairment of the epithelial differentiation program. The use of complex phytoadaptogen in the treatment of patients with leukoplakia normalized expression of Fas-APO-1 antigen and keratin 17; increased expression of CD54 attested to activation of immune effectors. The clinical effect manifested in involution or shrinkage and loosening of the pathological focus and complete epithelialization of erosive surfaces. The phytopreparation exhibited adaptogenic effects normalizing the immune and IFN status and improving the state of adaptation systems in the body.