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colony-stimulating factor (GM-CSF); IL-7, -9, -13, and -15; monocyte-CSF
(M-CSF); and stem cell factor (SCF). Long-chain hormone/CTKs include GH, PRL,
erythropoietin, thrombopoietin, leptin, IL6-11, LIF, OM, CNTF, cardiotrophin-1
(CT1), and G-CSF. Moreover, GH and PRL share the Jack3/Stat5(A,B) pathway of
signal transduction with type I CTKs [103-105] . This similarity raises the possibility
that GLH could in fact substitute for type I CTKs during immune function.
In contrast with CTKs, which are not present in the circulation in significant
quantities during health, PRL and GH are freely available in the serum. Further, the
development of naïve lymphocytes in the bone marrow, thymus, and spleen is depen-
dent on pituitary PRL and GH. It was also demonstrated that the primary antibody
response in young (100 g body weight) rats was dependent on pituitary hormones
when immunization was carried out without the use of immunological adjuvants.
This was true for cell-mediated, humoral immunity and autoimmune reactions. The
iron levels of anemic Hypox animals were also restored to normal by PRL, GH, and
placental lactogen [13,106,107] . Moreover, serum PRL regenerates in young (100 g
body weight) Hypox rats and reaches about 40% of normal by 6 weeks after opera-
tion. ADIM and bone marrow functions return to normal in such animals [108] . Here
it should be noted that during APR, pituitary GH and PRL are suppressed, yet the
bone marrow is hyperactive. Elevated levels of type I CTKs, such as GM-CSF and
IL-6, could mediate this alternate pathway of activation.
The IS develops memory cells gradually and secondary immune reactions become
independent of pituitary hormones. Current evidence suggests that type I CTKs play
a key role of maintaining memory cells [71] , which in turn play significant roles in
the maintenance of immune function during the adult life of animals and humans.
Memory cells have a remarkable capacity to survive crisis situations and regenerate
immune function after recovery from disease (see Section 1.4.1).
Many cells and tissues other than the pituitary make PRL, including immune
cells. PRL is synthesized by various subtypes of immune cells from humans, mice,
and rats, and immune-derived PRL is known to play a role in human autoimmune
disease [109] . However, lymphocyte-derived PRL is pituitary dependent [110] .
It is reasonable to suggest at this stage that in utero the IS relies on placental lac-
togens for development. After birth, pituitary GH, PRL, IGF-1, and the HPA axis are
involved in regulating immune function [111] . This applies to naïve lymphocytes of
the ADIM system. After priming with antigen, ADIM cells depend on type I CTKs
for their survival and function. This is the case also for memory cells. Type I CTKs
also support the HP and survival of naïve and memory T cells, naïve B cells, and NK
cells. However, in situations when CTKs are in short supply, such as severe radia-
tion disease for instance, and a number of other “stressful” conditions [112] , pitu-
itary GH and PRL are available right in the serum to perform the function of type I
CTKs and support the IS until it fully recovers. Clearly, GLH (GH, PRL, and placen-
tal lactogens) are involved in the development of the IS, including the bone marrow;
in the maintenance of naïve lymphocytes until they are primed with antigen (e.g.,
maintenance of immunocompetence); and in regeneration of immune function after
severe immunosuppressive insults to the body. Compelling experimental and clinical
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