Table 1 shows a summary of different studies providing scientific relevance regarding the effect of stress on the immune system.Table 1Relevant studies about the influence of psychological stress on the immune systemReferencesMain conclusionsOrtega M. 2006 Stress is a risk factor for health in all systems of the body; even though a certain level of stress is essential to boost productivity, once a limit is exceeded by an intense stressor, the body becomes depleted, causing stress-associated diseases.Rosenthal S. 2002 Ray O. 2004 Sierra R et al. 2006 Sandín B. 2008 McEwen B.S. 2008 An altered immune system caused by stressful events increases the body’s vulnerability (to infectious diseases, cancer and autoimmune diseases).Borysenko J, Borysenko M. 1983 Gidron Y et al. 2003 Ho W, Evans D, Douglas S. 2002 Social, physical, and biological factors that cause stress may induce immunosuppression, including inability to adapt to the environment, trauma, major surgical interventions, radiation, infection, and cancer.Monjan A, Collector M. 1977 Exposure to chronic stress induced proliferation of T and B lymphocytes similar to or to an even greater than a control treatment. Additionally, exposure of mice to acute noise stress for more than 2 to 3 h a day for fewer than 2 consecutive days reduced B and T lymphocyte proliferation in response to the mitogens lipopolysaccharide and concanavalin A, compared to non-exposure to stress.Fillion L et al. 1994 Weiss J et al. 1989 Hucklebridge F, Clow A, Evans P. 1998 Stress is related to increased viral retention in tissues, along with a decrease in the number of circulating lymphocytes and in the mitogenic response in vitro. In addition, stress diminishes the activity of natural killer (NK) cells, a powerful mechanism for the elimination of tumor cells and the production of interferon-γ.Moynihan J, Ader R, Crota L et al. 1990 Most immune responses are suppressed by stress, but moderately intense stress conditions can increase them.Croset G et al. 1987 Rat immune system reactivity was tested by determining the proliferative response after mitogenic stimulation in vitro as well as the capacity to generate a primary antibody response after immunization with red blood cells from sheep. An increase in the immune response in vitro and in vivo was demonstrated following exposure to a single shock. Thus, it was concluded that emotional stimuli facilitate immune responses. However, when a rat was confronted with a conflict situation, there was a decrease in the reactivity of the immune system. These findings led to the final conclusion that the immune system specifically and immediately reacts to different psychological stimuli.Shirinsky I, Shirinsky V. 2001 Belova T et al. 1988 Immune reaction initiation may be strongly affected by stress-induced cerebrovascular damage.Churin A et al. 2003 Immobilization stress induces different immune system reactions in distinct strains of rodents. These reactions can be classified according to the intensity of the humoral immune response for thymus-dependent antigens into categories such as high, moderate and low responders. High and moderate responders are characterized by high sensitivity of the productive phase of the humoral immune response and the phagocytic activity of macrophages. In low responders, stress only slightly affected the productive phase of the humoral immune response, but peritoneal macrophage activity decreased. This evidence reflects the different reactions of the immune system.De Groot J et al. 2002 This study of stress revealed the consequences of stress on the quality and quantity of immunological memory in the long term. Mice were subjected to social stress after herpes simplex virus infection. Stressed mice were shown to exhibit suppressed antibody response and impaired memory for the production of IL4 and IL10 as a specific response to the virus, whereas non-stressed mice showed intact immune responses and immune memory.Guayerbas N et al. 2002 This study found that on standard behavioral tests, rodents with high levels of anxiety had less competition in their immune system (premature immunosenescence), as demonstrated by certain functional alterations of peritoneal macrophages, such as substrate adherence, chemotaxis, phagocytosis, and superoxide anion production.Zelena D et al. 2003 In rats subjected to stress by repeated trapping, chronic stress signs including decreased thymus size and weight, increased adrenal gland weight, and increased basal corticosterone levels were observed.Molina P. 2001 Studies in rats subjected to hemorrhagic shock stress showed a suppressive role of noradrenergic innervation in the increase in tissue TNF-α levels initiated by hemorrhage in vivo. Therefore, it was concluded that norepinephrine protects against tissue damage but may contribute to generalized immunosuppression following trauma.Wonnacott K, Bonneau R. 2002 In a murine model, stress reduced the ability of specific cytotoxic memory T lymphocytes to protect against lethal intranasal or intravaginal infection with a herpes simplex virus. Stress also restricted the ability of these lymphocytes to limit virus levels at the site of the infected mucosa.Paltrinieri S et al. 2002 The efficiency of granulocytes was studied in sheep subjected to acute stress, and the results demonstrated that acute stress significantly increased the adhesion of these cells. This mechanism could be responsible for the depression of innate immunity observed in stressed animals.Sánchez M, Cruz C. 1991 Human studies revealed that IgA class antibodies, which are important in the defense against viruses and bacteria, had reduced abundance in individuals with a particular personality type.Stowell J. 2003 In humans, certain academic examinations can have a noteworthy impact on mental and physical health.Matalka K. 2003 A review of mental stress models (short and written examinations as subacute and acute types of stressors) was conducted to understand the effects of stress on the neuroendocrine and immune systems. In stressed students, a short period (minutes) of preparation for a written exam induced the production of proinflammatory cytokines, which could be related to a Th1 response. Nevertheless, prolonged mental stress (of several days) caused deregulation of immune function, with a change in the cytokine response to a Th2 response.Anyanwu E et al. 2003 Abnormal NK cell activity was found in patients exposed to toxigenic materials, leading to adverse health conditions, including a wide range of neuroimmune and behavioral consequences.Ho C et al. 2001 Measurable changes in dendritic cell abundance were observed in patients undergoing surgery. These cells were rapidly mobilized in the circulation in response to surgical stress, and this activity may prepare host immune defenses against trauma.Woiciechowsky C et al. 1998 In patients with sympathetic activation due to acute accidental brain trauma, rapid systemic release of the anti-inflammatory cytokine IL10 from non-stimulated monocytes occurs. The rapid release of this cytokine may signify a common pathway for stress-induced immunosuppression.Dhabhar F, McEwen B. 1999 Divergent from the concept that stress impairs immunity, human studies showed that short-term stressors pointedly increase delayed hypersensitivity reactions of skin.Glaser R. 2005 Individuals exposed to chronic diseases are more likely to present deleterious health and hygiene habits compared to individuals who do not have stress, such as sleep disturbances, malnutrition, physical inactivity and drug and tobacco abuse; thus enhancing the adverse effects of stress on the immune system and overall health.Levitina E. 2001 Immunological studies in infants who suffered from perinatal hypoxic stress demonstrated impaired cellular immunity (lymphocyte subpopulations) and humoral immunity (immunoglobulin concentrations). Acute hypoxia led to transient immunodeficiency due to stress.Ramos, V et al. 2008 Chronic and excessive stimulation of the hypothalamic-pituitary-adrenal axis induces the production of glucocorticoids, the final products of this axis, altering the levels of white blood cells, decreasing the activity of NK cells and inhibiting the production and secretion of ILs that are important in mediating the immune response.Mohr D, Pelletier D. 2004 Stress in individuals with multiple sclerosis increases the permeability of the blood–brain barrier to immune cells circulating in the blood. As a result, there is an increase in the infiltration of leukocytes into the CNS.Selye H. 1936 Hypotrophy of the thymus and lymph nodes was demonstrated after exposure to stress. The immunomodulatory effect of glucocorticoids is essential to this effect.Kay G et al. 1998 Prenatal stress from maternal isolation and exposure to noise and intense light during the last week of gestation in rats reduced the proliferative response of B lymphocytes and decreased the cytotoxic activity of NK cells in peripheral blood.Spitzer et al. 2010 People diagnosed with post-traumatic stress disorder were found to be significantly more likely to have elevated C-reactive protein levels.Gill J, Page G 2008 Gola et al. 2013 Sutherland, A., Alexander, D. Hutchison, J.2003 von Kanel et al. 2006 von Kanel et al. 2007 Baker et al. 2001 Maes et al. 1999 Newport D, Nemeroff C. 2000 Research showed that people with post-traumatic stress disorder have elevated levels of proinflammatory cytokines, especially IL6, which has been considered a potential prognostic biomarker for this pathology.Gotovac et al. 2010 Pace et al. 2012 Evidence was found for cytotoxic changes to NK cells in people with post-traumatic stress disorder, as well as an increase in the number of glucocorticoid receptors on lymphocytes and a decrease in the sensitivity to glucocorticoids.Cohen et al. 2001 Herbert T, Cohen S. 1993 Reduced NK cell cytotoxicity, suppressed lymphocyte proliferative responses, and blunted humoral responses to immunization were found in chronic stress models.Montoro J et al. 2009 Activation of the neuroendocrine and sympathetic nervous systems through catecholamine and cortisol secretion influences the immune system, modifying the balance between Th1 and Th2 responses in favor of the Th2 response.