Journal of Immunotoxicology

ISSN: 1547-691X (Print) 1547-6901 (Online) Journal homepage: https://www.tandfonline.com/loi/iimt20

Personality, Coping Style, and Constitutional

Neuroimmunology

Andrey A. Zozulya, Marina V. Gabaeva, Oleg Yu. Sokolov, Ida D. Surkina &
Natalia V. Kost

To cite this article: Andrey A. Zozulya, Marina V. Gabaeva, Oleg Yu. Sokolov, Ida D. Surkina &
Natalia V. Kost (2008) Personality, Coping Style, and Constitutional Neuroimmunology, Journal of
Immunotoxicology, 5:2, 221-225, DOI: 10.1080/15476910802131444

To link to this article: https://doi.org/10.1080/15476910802131444

Published online: 09 Oct 2008.

Submit your article to this journal

Article views: 985

View related articles

Citing articles: 34 View citing articles

Full Terms & Conditions of access and use can be found at

https://www.tandfonline.com/action/journalInformation?journalCode=iimt20
Journal of Immunotoxicology, 5:221–225,
Copyright
c Informa Healthcare USA, Inc.
ISSN: 1547-691X print / 1547-6901 online
DOI: 10.1080/15476910802131444
REVIEW ARTICLE
Personality, Coping Style, and Constitutional
Neuroimmunology
Andrey A. Zozulya, Marina V. Gabaeva, Oleg Yu. Sokolov, Ida D. Surkina,
and Natalia V. Kost
National Center for Mental Health, Russian Academy of Medical Sciences, Moscow, Russia
Risk of developing certain diseases correlates with human per-
sonality. Cardiologists have defined Type “A” personalities as
coronary-prone. Associated psychological peculiarities are easily
angered, competitive, impatient and hard-driving. Psychologically-
opposite people who are prone to suppress emotions and avoid con-
flicts (Type “C”), have a high risk of infectious diseases and certain
forms of cancer. The development of contemporary biology and
medicine determined an important role of the neuroendocrine and
immune systems in these correlations. The peculiarity of human
personality, as much as of animal behavioral patterns, is strongly
expressed under stress conditions. The strategies of stress coping
display a normal distribution in the human and wild animal popula-
tions, with truly passive and active coping styles located at the outer-
most regions of the curve. However, there are a number of strategies
to breed experimental animals with extreme coping styles; animals
selected for a passive coping style to acute stress show marked ac-
tivation of the hypothalamic-pituitary-adrenal (HPA) axis and low
stimulation of the sympathetic-adrenal system; both are associated
with immunosuppression. An opposite reaction of the neuroen-
docrine system has been shown in animals with an active coping
style to stress; this was associated with the signs of immunostimula-
tion. Similarly, people with passive coping style (type “C”) might be
at higher risk of infectious diseases and cancer, while people with
active coping style (type “A”) might be predisposed to coronary,
allergic, and autoimmune diseases. Furthermore, pain, decreased
productivity, and anxiety, all common in patients with different
diseases, are additional stressful entities. Thus, an adequate coping
with a disease is an important approach to improve life quality and
disease prognosis. Therefore, psychological and psychopharma-
cotherapeutic interventions that enhance effective coping should
have beneficial effects in patients with immune-mediated diseases.
Keywords Personality, coping style, neuroendocrine system, im-
mune system
PERSONALITY AND COPING STYLES
It is well known from the time of Hippocrates that the risk
of development of certain diseases correlates with the type of
Received 10 December 2007; accepted 4 February 2008.
Address correspondence to Dr. Natalia V. Kost, National Center
for Mental Health, Russian Academy of Medical Sciences, Moscow,
Russia; e-mail: nat-kost@yandex.ru
221
human personality. In this connection, Hippocrates marked out
four types of temperament: melancholic, choleric, phlegmatic,
and sanguine. Half a millennium later, Galenos picked out the
melancholicus as being prone to cancer. Later, people with be-
havior patterns such as denial, suppression of emotions (anger
primarily), avoidance of conflicts, social desirability, harmoniz-
ing behavior, high rationality were shown to have a high risk
of infectious diseases, certain forms of cancer and they were
termed type “C” (Baltrusch et al., 1991). In contrast, a Type “A”
personality has been defined by cardiologists as coronary-prone.
Psychologically, people of this type are hostile, easily angered,
competitive, impatient and hard driving (Friedman et al., 1975;
Irvine et al., 1982). The correlation between the people person-
ality and their susceptibility to certain disorders has been sup-
ported by contemporary data on constitutional neurochemistry,
neuroendocrinology, and neuroimmunology.
The development of contemporary biology and medicine al-
lowed the characterization of the molecular mechanisms in-
volved in the regulation of susceptibility of people with dif-
ferent personality types to a number of diseases and determined
an important role of the neuroendocrine and immune systems in
this relationship. Specific biological feature of type “A” people
is the high sympathetic system activity caused, in part, by the
elevated sensitivity of β-adrenoreceptors (Catipovič-Veselica
et al., 1997; Le Melledo et al., 2001) and increased blood cate-
cholamine levels (Friedman et al., 1975). High urine testosterone
is also typical for type “A” people (Zumoff et al., 1984).
The specificity of human personality, as well as animal behav-
ioral patterns, is strongly expressed under the stress conditions.
There are plenty of behavioral and psychological methods to
evaluate the stress coping strategy, i.e., coping style, in human
and animals. These styles are distinguished as flight/fight, re-
pressive/defensive, submissive/aggressive, anger-in/anger-out,
blunting/monitoring, negative/positive, etc. (Jamner at al., 1988;
De Boer et al., 1990; Zozulya et al., 1996; Devoino et al., 2003;
Veenema et al., 2004). In general, coping styles might be grouped
into “passive” and “active” patterns. The strategies of stress cop-
ing display normal distribution in the overall human and wild
222 ZOZULYA ET AL.
TABLE 1
The reaction of the HPA-axis and SAS to acute experimental stress in animals selected to “active” (A) and “passive” (P) coping
styles by different behavioral patterns
Behavioral model
Locomotion (open field), Seredenin et al. (1983, 2003)
Avoidance (shuttle-box), Steimer and Driscoll (2003) De Boer et al. (1990)
Aggression (attack latency), Veenema et al., 2004 Sgoifo et al. (1996)
Anxiety (social defeat), Frank et al. (2006)
A < P – the level of corresponding hormone in animals with “active” coping style was lower as compared to “passive” ones, and vice-versa.
ND - not determined.
animal populations, with truly “passive” and “active” coping
styles located at the outermost regions of the curve. In order to
study the biological pattern of the phenomenon, researchers usu-
ally select animals with extreme coping styles by their behavior
under the different stress conditions.
Coping Styles and Neuroimmunoendocrinology
Using a number of behavioral models, it has been shown
that coping style determines, to a large degree, the reaction of
the neuroendocrine system to stress. For instance, animals se-
lected for the “passive” coping style (in the “open field,” “shuttle-
box” or some zoo social models) show marked activation of the
hypothalamic-pituitary-adrenal axis (HPA) and low stimulation
of the sympathetic adrenal system (SAS) in response to acute
stress (Table 1). This has been demonstrated by analyzing the
levels of adrenocorticotropic hormone (ACTH), corticosterone
and norepinephrine in the blood of animals under the stress con-
ditions. It should be noted that under the rest conditions, basal
levels of corticosterone in “passive” animals might be lower
as compared to the levels in “active” animals. However, acute
stress induces more pronounced rise of the hormone level, which
is accompanied by rapid exhaustion of HPA in “passive” animals
(De Boer et al., 1990; Seredenin, 2003; Steimer and Driscoll,
2003; Veenema et al., 2004; Frank et al., 2006). An opposite
reaction of the HPA and SAS systems has been demonstrated
in animals with the “active” coping style. They show relatively
low release of ACTH and corticosterone, but with high levels of
catecholamines in the blood following acute stressful stimulus
(Table 1; De Boer et al., 1990; Sgoifo et al., 1996).
The stress reaction of the immune system has being stud-
ied since the past century. In many experimental models it was
shown that, as a rule, acute stress induced some signs of im-
mune stimulation, while chronic stress induced immunosup-
pression (Korneva and Shkhinek, 1989; Shurin et al., 1994). A
meta-analytic study of 30-year inquiry permitted Segerstrom and
Miller (2004) to pick out different stages of the human immune
system changes under the psychological stress. Acute stressors
(lasting minutes) were associated with potentially adaptive up-
regulation of natural immunity and down-regulation of adaptive
immune responses. Brief psychological stressors (such as an
exam) tended to suppress cellular immunity while preserving
ACTH Corticosterone Norepinephrine
A<P A<P ND
A < P, ND A<PA<P ND, A > P
A < P, ND A < P, ND ND, A > P
ND A<P ND
humoral immunity. Chronic stressors were associated with sup-
pression of both cellular and humoral immune responses. One
might forecast that stress perception depends on the human per-
sonality, stress coping style, which, as has been shown above,
might determine the neuroendocrine stress reaction.
Neuroendocrine immunomodulation is achieved through
both autonomic innervation of immune system organs and hor-
monal receptors on immune cells (Sternberg, 2006). For ex-
ample, dendritic cells, which are the key regulators of in-
nate and adaptive immunity, bear receptors to biogenic amines
(i.e., α1A, β1, β2-adrenoreceptors (Maestroni, 2005), 5-HT-
receptors (Idzko et al., 2004)), steroids (i.e., glucocorticoid re-
ceptors) (Bellinghausen et al., 2001; Freeman et al., 2005), and to
regulatory peptides (i.e. δ-, µ-, κ-opioid receptors) (Eshe et al.,
1999; Kirst et al., 2002). Therefore, the balance between the
levels of different stress-realizing hormones should be impor-
tant for the degree and even direction of the immunomodulative
stress reaction.
Animal Studies
It would be important now to analyze the associations be-
tween the neuroendocrine reaction to stress in human and an-
imals with “passive” and “active” stress coping style and the
stress-reaction of the immune system. We have shown that un-
der the stress conditions Wistar rats with “passive” strategy in
“AutoTrack System” have low proliferative responses of blood
lymphocytes to the mitogen Conconavalin A as compared to
“active” ones. It should be mentioned that treatment with a syn-
thetic analog of the opioid peptide Leu-enkephalin (dalargin)
normalized this stress reaction, meaning that lymphocyte pro-
liferation was heightened in “passive” animals and decreased
in “active” rats (Zozulya et al., 1996). This fact provides addi-
tional support for a homeostatic role of regulatory peptides un-
der stress conditions. Similarly, low-active in “open field” Lewis
rats have lower mitogen-induced interleukin (IL)-10 and inter-
feron (IFN)-γ production by splenocytes (Sajti et al., 2004).
It is well known that Balb/c mice display “passive” behavior
in “open field” and have lower humoral and higher cellular
immune responses than the “active” in “open field” C57Bl/6
mice (Seredenin, 2003). Also, the exploratory behavior of (CBA
× C57Bl/6)F1 mice in “open field” correlates with a delayed-
type hypersensitivity, proliferative activity of immune cells, and
 PERSONALITY, COPING STYLE AND CONSTITUTIONAL NEUROIMMUNOLOGY
expression of the IL-1β‚ type I IL-1 receptor, and erythropoietin
receptor genes in brain cells (Markova et al., 2000, 2004).
Aggression is another behavioral pattern to select the strat-
egy of stress coping in animals. It has been shown that low-
aggressive (“passive” strategy) wild house mice have faster
thymus involution under defeat stress (Veenema et al., 2004).
Moreover, acute stress induces immune stimulation in “aggres-
sive” and immunosuppression in “submissive” C57Bl/6J mice
(Devoino et al., 2003).
Human Studies
An interconnection of personality, coping style and immune
status has been also demonstrated in human. The “passive” cop-
ing style is associated with decreased monocyte numbers, el-
evated eosinophile counts (Jamner et al., 1988), and a stress-
induced decrease in T-helper lymphocytes (Sakami et al., 2004).
The type of character accentuation relates to humoral immunity
(Zabrodskii and Timofeev, 1997; Abramov et al., 2001). The
personality tested by MMPI is connected to NK activity and the
ratio of T-lymphocyte subpopulations (Biondi et al., 1994). High
introversion, together with high neuroticism, which is typical for
a melancholic temperament (Eysenck, 1967) and for “passive”
coping style, is associated with low IFN„ production by blood
lymphocytes (Surkina et al., 2001).
Personality, Coping Style and Immune-Mediated Diseases
Thus, the “passive” acute stress coping style exhibits marked
activation of HPA axis and low stimulation of SAS, both associ-
ated with signs of immunosuppression. This type of personality
in people is a risk factor for infectious diseases and some forms
of cancer (Jamner et al., 1988; Baltrusch et al., 1991; Sakami
et al., 2004). An opposite reaction of the HPA and SAS systems
to stress has been demonstrated in animals with an “active” stress
coping style. It was associated with up-regulated function of the
immune system, as well. Depletion of SAS on a background of
low cortisol under chronic stress might however induce hyper
activation of the immune system in people with “active” coping
style. This can raise the risk of inflammatory and autoimmune
diseases, including arthritis, systemic lupus erythematosus, al-
lergy, asthma, atopic dermatitis, etc. (Wilder, 2002; Marques-
Deak et al., 2005).
In fact, particular features of temperament and behavior have
been found in children with allergy and asthma in a pre-morbid
period (Kim et al., 1980; Lilljeqvist et al., 2002; Stevenson
et al., 2003). High liability was shown to be typical for adults
with atopic dermatitis (Scheich et al., 1993). One study, per-
formed with a large sampling (n = 11,540), has shown that high
extra-version is a risk factor for asthma in women (Huovinen et
al., 2001). A reduced activity of the HPA axis in patients pre-
disposed to allergic diseases was confirmed by low basal and
stress-induced blood cortisol levels (Buske-Kirschbaum et al.,
2003) and saliva (Ball et al., 2006). A peculiarity of the SAS
function has been shown in children with asthma (Miller and
223
Chen, 2006) and patients with systemic lupus erythematosus
(Pawlak et al, 1999). A high basal level of β2 -receptors expres-
sion was detected in lymphocytes; a reduction of this param-
eter was more pronounced in above-mentioned patients under
the psychoemotional stress as compared to healthy volunteers.
Moreover, the immunomodulating effect of adrenalin in patients
with rheumatoid arthritis differed from that in healthy people.
This was shown during the analyses of levels of NK cell activ-
ity, T-lymphocyte subpopulations, and pro-/anti-inflammatory
cytokine production in these populations (Kittner et al., 2002).
CONCLUSIONS
Thus, the reactivity of the nervous system to stress deter-
mines, to certain degree, a stress reaction of other systems such
as the cardiovascular and the immune system (Figure 1). This
reaction is mediated by the neuroendocrine system, partly by
the ratio of HPA axis and SAS activity. As a result, people with
a “passive” coping style (type “C”) might be under a higher
risk of infectious diseases and cancer, while people with an “ac-
tive” coping style (type “A”) might be predisposed to coronary,
allergic and autoimmune diseases.
Furthermore, symptoms such as pain, decreased productiv-
ity, and anxiety, which are common in patients with differ-
ent diseases, comprise additional stressful entities. Thus, ad-
equate and efficient coping with the disease is an important
approach to improve the life quality of patients and the dis-
ease prognosis. For instance, the global health-related quality
of life positively correlates with an “active” coping style in pa-
tients with different types of cancer (Zhou et al., 2005). Psy-
chological and psycho-pharmacotherapeutic interventions that
enhance an effective coping have shown beneficial effects in can-
cer patients (Reiche et al., 2005). Moreover, one could suggest
that the stress of environment pollution would induce different
immune-mediated disease development in persons with different
personalities.
Since the coping style is the result of the interplay between
an innate predisposition and environmental and social factors,
Passive Active
N
total population
Infections and Cardiovascular,
cancers allergic, and
autoimmune
diseases
HPA > SAS HPA < SAS
The reactivity of the nervous, immune, and cardiovascular systems
FIG. 1. Personality, coping style and predisposition to immune-mediated dis-
eases. HPA = hypothalamic-pituitary-adrenal axis; SAS = sympathetic-adrenal
system.
224 ZOZULYA ET AL.
it can be corrected. Psychological and psychopharmacological
correction of a particular coping style may be beneficial for both
decreasing the susceptibility to immune-mediated diseases and
optimizing the efficacy of immunotherapy.
REFERENCES
Abramov, V. V., Markova, E. V., Poveshchenko, A. F., Gontova, I. A.,
Yakushenko, E. V., Korotkova, N. A., Abramova, T. Y., and Kozlov, V. A.
2001. The interdependence of behavior and immunity: Possible mechanisms
and significance. Russ. J. Immunol. 6:215–220.
Ball, T. M., Anderson, D., Minto, J., and Halonen, M. 2006. Cortisol circadian
rhythms and stress responses in infants at risk of allergic disease. J. Allergy
Clin. Immunol. 117:306–311.
Baltrusch, H. J., Stangel, W., and Titze, I. 1991. Stress, cancer and immu-
nity. New developments in biopsychosocial and psychoneuroimmunologic
research. Acta Neurol. (Napoli) 13:315–327.
Bellinghausen, I., Brand, U., Steinbrink, K., Enk, A. H., Knop, J., and Saloga, J.
2001. Inhibition of human allergic T-cell responses by IL-10-treated dendritic
cells: Differences from hydrocortisone-treated dendritic cells. J. Allergy Clin.
Immunol. 108:242–249.
Biondi, M., Peronti, M., Pacitti, F., Pancheri, P., Pacifici, R., Altieri, I., Paris,
L., and Zuccaro, P. 1994. Personality, endocrine and immune changes after
eight months in healthy individuals under normal daily stress. Psychother.
Psychosom. 62:176–184.
Buske-Kirschbaum, A., von Auer, K., Krieger, S., Weis, S., Rauh, W., and
Hellhammer, D. 2003. Blunted cortisol responses to psychosocial stress in
asthmatic children: A general feature of atopic disease? Psychosom. Med.
65:806–810.
Catipovič-Veselica, K., Durijancek, J., Bracič-Kalan, M., Amidzič, V., Mrde-
novič, S., Kozmar, D., Burič, D., and Catipovič, B. 1997. Heart rate and
heart-rate variability in patients with acute coronary heart disease classified
on Bortner’s scale as type A and type B. Psychol. Rep. 80:775–784.
De Boer, S. F., Slangen, J. L., and Van der Gugten, J. 1990. Plasma catecholamine
and corticosterone levels during active and passive shock-prod avoidance
behavior in rats: Effects of chlordiazepoxide. Physiol. Behav, 47:1089–1098.
Devoino, L., Alperina, E., and Pavina, T. 2003. Immunological consequences
of the reversal of social status in C57Bl/6J mice. Brain Behav. Immunol.
17:28–34.
Eshe, C., Makarenkova, V. P., Kost, N. V., Lotze, M. T., Zozulya, A. A., and
Shurin, M. R. 1999. Functional δ-type opioid receptors on dendritic cells.
Ann. N.Y. Acad. Sci. 885:387–390.
Eysenck, H .J. (Ed.) 1967. The Biological Basis of Personality. Charles C.
Thomas Publishers: Springfield, IL.
Frank, E., Salchner, P., Aldag, J. M., Salomé, N., Singewald, N., Landgraf,
R., and Wigger, A. 2006. Genetic predisposition to anxiety-related behavior
determines coping style, neuroendocrine responses, and neuronal activation
during social defeat. Behav. Neurosci. 120:60–71.
Freeman, L., Hewison, M., Hughes, S. V., Evans, K. N., Hardie, D., Means, T. K.,
and Chakraverty, R. 2005. Expression of 11β-hydroxysteroid dehydrogenase
type 1 permits regulation of glucocorticoid bioavailability by human dendritic
cells. Blood 106:2042–2049.
Friedman, M., Byers, S. O., Diamant, J., and Rosenman, R. H. 1975. Plasma
catecholamine response of coronary-prone subjects (typeA) to a specific chal-
lenge. Metabolism 24:205–210.
Huovinen, E., Kaprio, J., and Koskenvuo, M. 2001. Asthma in relation to per-
sonality traits, life satisfaction, and stress: A prospective study among 11,000
adults. Allergy 56:971–977.
Idzko, M., Panther, E., Stratz, C., Müller, T., Bayer, H., Zissel, G., Dürk, T.,
Sorichter, S., Di Virgilio, F., Geissler, M., Fiebich, B., Herouy, Y., Elsner, P.,
Norgauer, J., and Ferrari, D. 2004. The serotoninergic receptors of human
dendritic cells: Identification and coupling to cytokine release.J. Immunol.
172:6011–6019.
Irvine, J., Lyle, R. C., and Allon, R. 1982. Type A personality as the psy-
chopathology: Personality correlates and an abbreviated scoring system. J.
Psychosom. Res. 26:183–189.
Jamner, L. D., Schwartz, G. E., and Leigh, H. 1988. The relationship between
repressive and defensive coping styles and monocyte, eosinophile, and serum
glucose levels: support for the opioid peptide hypothesis of repression. Psy-
chosom. Med. 50:567–575.
Kim, S. P., Ferrara, A., and Chess, S. 1980. Temperament of asthmatic children.
A preliminary study. J. Pediatr. 97:483–486.
Kirst, A. Wack, C., Lutz, W. K., Eggert, A., Kämpgen, E., and Fischer, W. H.
2002. Expression of functional κ-opioid receptors on murine dendritic cells.
Immunol. Lett. 84:41–48.
Kittner, J. M. Jacobs, R., Pawlak, C. R., Heijnen, C. J., Schedlowski, M.,
and Schmidt, R. E. 2002. Adrenaline-induced immunological changes
are altered in patients with rheumatoid arthritis. Rheumatology 41:1031–
1039.
Korneva, E. A., and Shkhinek, E. K. 1989. Stress and immune system function.
Usp. Fiziol. Nauk. 20:3–20.
Le Mellédo, J. M., Arthur, H., Dalton, J., Woo, C., Lipton, N., Bellavance,
F., Koszycki, D., Boulenger, J. P., and Bradwejn, J. 2001. The influence of
type A behavior pattern on the response to the panicogenic agent CCK-4. J.
Psychosom. Res. 51:513–520.
Lilljeqvist, A. C., Smørvik, D., and Faleide, A. O. 2002. Temperamental differ-
ences between healthy, asthmatic, and allergic children before onset of illness:
A longitudinal prospective study of asthma development. J. Genet. Psychol.
163:219–227.
Maestroni, G. J. 2005. Adrenergic modulation of dendritic cells function: Rel-
evance for the immune homeostasis. Curr. Neurovasc. Res. 2:169–173.
Markova, E. V., Chernova, T. G., Fillimonov, P. N., Korotkova, N. A., Abramov,
V. V., and Kozlov, V. A. 2004. Immunomorphological characteristics of ani-
mals with different levels of orientation and exploratory behavior. Bull. Exp.
Biol. Med. 138:415–417.
Markova, E. V., Gromykhina, N. Y., Abramov, V. V., and Kozlov, V. A. 2000. The
peculiarities of the immune status in mice with different level of behavioral
reactions. Russ. J. Immunol. 5:89–94.
Marques-Deak, A., Cizza, G., and Sternberg, E. 2005. Brain-immune interac-
tions and disease susceptibility. Mol. Psych. 10:239–250.
Miller, G. E., and Chen, E. 2006. Life stress and diminished expression of genes
encoding glucocorticoid receptor and β2-adrenergic receptor in children with
asthma. Proc. Natl. Acad. Sci. USA 103:5496–5501.
Pawlak, C. R., Jacobs, R., Mikeska, E., Ochsmann, S., Lombardi, M. S.,
Kavelaars, A., Heijnen, C. J., Schmidt, R. E., and Schedlowski, M. 1999.
Patients with systemic lupus erythematosus differ from healthy controls in
their immunological response to acute psychological stress. Brain Behav. Im-
munol. 13:287–302.
Reiche, E. M., Morimoto, H. K., and Nunes, S. M. 2005. Stress and depression-
induced immune dysfunction: Implications for the development and progres-
sion of cancer. Int. Rev. Psych. 17:515–527.
Sajti, E., Van Meeteren, N., Kavelaars, A., van der Net, J., Gispen, W. H., and
Heijnen, C. 2004. Individual differences in behavior of inbred Lewis rats
are associated with severity of joint destruction in adjuvant-induced arthritis.
Brain Behav. Immunol. 18:495–496.
Sakami, S., Maeda, M., Maruoka, T., Nakata, A., Komaki, G., and Kawamura,
N. 2004. Positive coping up- and down-regulates in vitro cytokine produc-
tions from T-cells dependent on stress levels. Psychother. Psychosom. 73:243–
251.
Scheich, G., Florin, I., Rudolph, R., and Wilhelm, S. 1993. Personality charac-
teristics and serum IgE level in patients with atopic dermatitis.J. Psychosom.
Res. 37:637–642.
Segerstrom, S. C., and Miller, G. E. 2004. Psychological stress and the human
immune system: A meta-analytic study of 30 years of inquiry. Psychol. Bull.
130:601–630.
Seredenin, S. B. 2003. Genetic differences in response to emotional stress and
tranquilizers. Psichofarmacol. Biol. Narcol. 3:494–509.
 PERSONALITY, COPING STYLE AND CONSTITUTIONAL NEUROIMMUNOLOGY
Seredenin, S. B., Badyshtov, B. A., Nikitina, M. M., and Rozen, V. B. 1982.
Changes in the corticosterone content in the blood plasma of inbred mice
after stress exposure. Bull. Eksp. Biol. Med. 94:36–37.
Sgoifo, A., De Boer, S. F., Haller, J., and Koolhaas, J. M. 1996. Individ-
ual differences in plasma catecholamine and corticosterone stress responses
of wild-type rats: Relationship with aggression. Physiol. Behav. 60:1403–
1407.
Shurin, M. R., Zhou, D., Kusnecov, A., Rassnick, S., and Rabin, B. S. 1994.
Effect of one or more footshocks on spleen and blood lymphocyte proliferation
in rats. Brain Behav. Immunol. 8:57–65.
Steimer, T., and Driscoll, P. 2003. Divergent stress responses and coping styles
in psychogenetically selected Roman high-(RHA) and low-(RLA) avoidance
rats: Behavioral, neuroendocrine, and developmental aspects. Stress 6:87–
100.
Sternberg, E. 2006. Neural regulation of innate immunity: A coordinated non-
specific host response to pathogens. Nat. Rev. Immunol. 6:318–328.
Stevenson, J., and the ETAC Study Group. 2003. Relationship between behavior
and asthma in children with atopic dermatitis. Psychosom. Med. 65:971–
975.
Surkina, I. D., Yu Sokolov, O, Gabaeva, M. V., Gurevich, K. G., Alfimova,
M. V., Akatova, E. V., and Pak, L. S. 2001. Relationship between IFNγ
production by blood lymphocytes and constitutional personality features of
225
patients with idiopathic mitral valve prolapse. Bull. Exp. Biol. Med. 131:389–
391.
Veenema, A. H., Koolhaas, J. M., and De Kloet, E. R. 2004. Basal and stress-
induced differences in HPA axis, 5-HT responsiveness, and hippocampal cell
proliferation in two mouse lines. Ann. N.Y. Acad. Sci. 1018:255–265.
Wilder, R. L. 2002. Neuroimmunoendocrinology of the rheumatic diseases: Past,
present, and future. Ann. N.Y. Acad. Sci. 966:13–19.
Zabrodskii, P. F., and Timofeev, D. A. 1997. Relationship between the type of
character accentuation and indices of humoral immunity. Bull. Eksp. Biol.
Med. 124:70–72.
Zhou, F. L., Zhang, W. G., Wei, Y. C., Xu, K. L., Hui, L. Y., Wang, X. S., and
Li, M. Z. 2005. Impact of comorbid anxiety and depression on quality of life
and cellular immunity changes in patients with digestive tract cancers. World
J. Gastroenterol. 11:2313–2318.
Zozulya, A. A., Kost, N. V., Toropov, A. V., Meshavkin, V. K., Butenko, O.
B., and Barsegyan, G. G. 1996. The dependence of immunomodulative and
behavioral effects of opioid peptide dalargin on the parameters of higher
nervous activity in rats. Immunologia 5:25–29.
Zumoff, B., Rosenfeld, R. S., Friedman, M., Byers, S. O., Rosenman, R. H., and
Hellman, L. 1984. Elevated daytime urinary excretion of testosterone glu-
curonide in men with the type A behavior pattern. Psychosom. Med. 46:223–
225.