Posted by: Indonesian Children | April 14, 2010

A Molecular Basis for Bidirectional : A SENSORY FUNCTION FOR THE IMMUNE SYSTEM

A Molecular Basis for Bidirectional Communication Between the Immune and Neuroendocrine Systems


Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama


Perhaps the most interesting conceptu: al advance that follows from many of these studies is the idea that a principal new function of the immune system may be to serve as a sensory organ. It has been proposed that the immune system may sense stimuli that are not recognized by the central and peripheral nervous systems (15). These stimuli have been termed noncogni-tive and include those things (i.e., bacteria, tumors, viruses, antigens, etc.) that would go unnoticed were it not for their recognition by the immune system. The recognition of such noncognitive stimuli by immunocytes is then converted into information, in the form of peptide hormones, lymphokines, and monokines, that is conveyed to the neuroendocrine system, and a physio­logical change occurs. Contrariwise, central and peripheral nervous system recognition of cognitive stimuli results in similar hormonal information being conveyed to and recognized by hormone receptors on immunocytes and an immunologic change results. It seems that the sensory function of the immune system mimics the neuroendocrine system in terms of a given stimu­lus evoking a particular set of hormones and hence physiological responses. If



Volume 69

this proves to be the case, then the pathophysiology that is associated with a particular infectious agent, antigen, or tumor could be related in part to the particular hormone or set of hormones that are produced by the immune system. For instance, lymphocyte-derived ACTH or IL 2 or macrophage-de-rived IL 1 or HSF acting alone or in concert may be responsible for the well-known increase in circulating corticosteroid levels observed during viral and bacterial infections. It would be most gratifying if in the future, for example, successful embryo implantation might be associated with lympho­cyte CG or alterations of thyroid function might be associated with lympho­cyte-derived TSH.

Certain experimental models and clinical observations would seem to support the above view. The finding that cells of the immune system are a source of secreted ACTH suggested that stimuli that elicit the leukocyte-de­rived hormone should not require a pituitary gland for an ACTH-mediated increase in corticosteroids. This seemed to be the case, since Newcastle dis­ease virus (NDV, an in vitro inducer of leukocyte ACTH) infection of hypo-physectomized mice caused a time-dependent increase in corticosterone pro­duction that was inhibitable by dexamethasone. Unless such mice were pre-treated with dexamethasone, their spleens were positive for ACTH by immunofluorescence (129). It should be noted that the possibility of an ex-trapituitary ACTH response in mice is currently an unsettled problem in that Dunn et al. (45) were unable to completely reproduce this finding. In this study, only a small proportion of verified hypophysectomized mice (4 of 47) showed a virus-induced increase in corticosterone. One important difference between the studies that could account for the discrepancy is the omission of a crucial control/Although the first study showed that the spleens of NDV-infected animals actually produced ACTH, the second did not verify spleno-cyte production of ACTH. In the more recent study, perhaps the small num­ber of verified hypophysectomized mice that showed corticosterone increases were the only ones that produced splenocyte ACTH. This is a particularly important control, since Dunn et al. (45) used a different and more virulent strain of NDV.

Another study that supports the concept of an extrapituitary ACTH response was performed in children with hypopituitarism. Children who were pituitary ACTH deficient were pyrogen tested (typhoid vaccine, another in vitro inducer of leukocyte ACTH) and were shown to have an increase in the percentage of ACTH-positive mononuclear leukocytes (99). Both the re­sponse in hypophysectomized mice and hypopituitary children peaked at ~6-8 h after administration of virus and typhoid vaccine, respectively. These findings might also explain the earlier observation of bacterial polysaccha-ride (piromen)-induced cortisol responses in seven of eight patients who underwent pituitary stalk sectioning (142). More recently, a patient pre­sented with the clinical and laboratory features of the ectopic ACTH syn­drome. Whereas the absence of a gradient in ACTH concentration between the inferior petrosal sinuses and the periphery argued against pituitary overproduction, no ACTH-producing tumor was found, and bilateral adrenal-



ectomy was performed to correct the hypercortisolism. Six months later, a pseudotumor containing only normal fat and inflammatory tissue was ob­served in the patient. On removal of this inflammatory tissue, basal plasma ACTH levels immediately returned to normal and leukocytes within the inflammatory tissue stained positively for ACTH by an immunoperoxidase procedure (46).

A possible in vivo corollary of the aforementioned ability of CRF and AVP to elicit in vitro ACTH was also observed (130). We found an increase in the percentage of circulating immunoreactive ACTH-positive leukocytes in normal short children who were undergoing assessment of pituitary function by insulin tolerance testing (99). In contrast to the previously described peak in the percentage of ACTH-positive leukocytes that occurred at 6-8 h post-typhoid vaccination, the peak was observed at 45-60 min after the adminis­tration of insulin. If both the in vivo and in vitro data are considered, it is tempting to speculate that in stressful situations leukocytes may produce ACTH in response to an encounter with CRF, which perhaps occurs as these cells pass through the portal circulation between the hypothalamus and pituitary gland. More recently it has been shown that CRF administration to pituitary ACTH-deficient individuals results in both an ACTH and cortisol response (50), and their leukocytes are positive for ACTH (H. L. Fehm, personal communication).

Gram-negative bacterial infections and endotoxin shock may represent yet another situation in which leukocyte production of hormones play a pivotal role. For instance, endorphins have been implicated in the pathophys-iology associated with these maladies since the opiate antagonist, naloxone, improved survival rates and blocked a number of cardiopulmonary changes associated with these conditions (115). Furthermore, two separate pools of endorphins have been observed after endotoxin administration, and it was suggested that one pool might originate in the immune system (33). If the potent immunologic effects of endotoxin are considered, as well as its ability to induce in vitro leukocyte production of endorphins, cells of the immune system seem the most likely source of endogenous opiates that are observed during Gram-negative sepsis and endotoxin shock. Consistent with this idea is the observation that lymphocyte depletion, like naloxone treatment, blocked a number of endotoxin-induced cardiopulmonary changes (23). Our interpretation of these results is that lymphocyte depletion removes the source of the endorphins, whereas naloxone blocks their effector function. Thus this may represent a situation in which leukocyte-derived endorphins are involved in a disease state as a manifestation of the sensory function of the immune system.


The recent observations of neuroendocrine peptide hormones and their receptors in and on leukocytes seem to now provide a molecular basis for the numerous interactions between the immune and neuroendocrine systems



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(21). With such findings, it appears a new scientific discipline has emerged, i.e., neuroimmunoendocrinology. New functions for these two systems, as well as novel conceptions of how each system perceives itself and one an­other, seem evident. Further knowledge of the interactions of these two systems at a molecular level should provide many new insights into neuroen-docrine and psychological disorders as well as the pathophysiology of infec­tious diseases and tumors. For instance, leukocyte ACTH, IL 1, IL 2, and HSF may be responsible for the well-known increases in corticosteroid levels ob­served during infections, and leukocyte ACTH certainly explains at least one instance of “ectopic” ACTH syndrome. Novel treatments for human diseases are also suggested, and the efficacy of naloxone in Gram-negative sepsis may represent the first example.

It is our feeling that perhaps one of the first major applications of this knowledge will be in the area of psychiatry. For instance, if brain receptors are important in behavior and are expressed with fidelity on white blood cells, then there is an easily accessible peripheral source to study more cen­trally located receptors. Correlations of aberrant leukocyte receptor numbers or functions may ultimately be diagnostic for psychological diseases. Thus this may lead to more objective type evaluations of psychiatric disorders. Future possibilities might also include correction of pituitary hormone defi­ciencies by an action of hypothalamic-releasing factors on leukocytes or the correction of immunodeficiencies by treatment with neuroendocrine hor­mones. Regardless of the specific outcome, it seems clear that neuroimmu­noendocrinology will have a major impact on our understanding of physiol­ogy and consequent diagnosis, therapeusis, and prophylaxis of human diseases.

I am indebted to my former and present graduate students, postdoctoral fellows, and faculty colleagues for advancing the study of neuroimmunoendocrinology. I also thank Diane Weigent for typing this manuscript and for excellent editorial assistance.

These studies were supported in part by National Institute of Diabetes and Digestive and Kidney Diseases Grant DK-38024, Office of Naval Research Grant N00014-84-K-0486, Cancer Center Core Grant CA-13148, Triton Biosciences, and the James W. McLaughlin Foundation.


  1. ADAMS, F., J. R. QUESADA, and J. V. GUTTERMAN. Neuropsychiatric manifestations of human leukocyte in-terferon therapy in patients with cancer. J. Am. Med. Assoc. 252: 938-941,1984.
  2. ADER, R., and N. COHEN. Psychoneuroimmunology. Orlando, FL: Academic, 1981, p. 281.
  3. ALANEN, A., and 0. LASSILA. Deficient natural killer cell function in preeclampsia. Obstet. Gynecol. 60: 631-634,1982.
  4. ALVAREZ-MON, A., J. H. KEHRL, and A. S. FAUCI. A potential role for adrenocorticotropin in regulating human B lymphocyte functions. J. Immunol. 135: 3823-3826,1985.
  5. BARONI, C. Thymus, peripheral lymphoid tissue, and immunological responsiveness of the pituitary dwarf mouse. Experientia Basel 23: 282-283,1967.
  6. BAR-SHAVIT, Z., S. TERRY, S. BLUMBERG, and R. GOLDMAN. Neurotensin-macrophage interaction: spe­cific binding and augmentation of phagocytosis. Neuro-peptides 2: 323-335,1982.
  7. BARTOCCI, A., V. PAPDEMETRION, E. SCHLICK, B. C. NISULA, and M. A. CHIRIGOS. Effect of crude and purified human chorionic gonadotropin on murine de­layed type hypersensitivity: a role for prostaglandins. Cell Immunol 71: 326-333,1982.
  8. BEACH, J. E., E. W. BERNTON, J. W. HOLADAY, R. C. SMALLRIDGE, AND H. G. FEIN. Interleukin-1 modu­lates secretion by cultured pituitary cells in monolayer culture (Abstract). Int Ccmgr. NeuroendocrinoL 1st San Francisco 1986, p. 106. 9. BERKENBOSCH, F., J. VAN OERS, A. DEL REY, F. TILDERS, and H. BESEDOVSKY. Corticotropin-re-leasing factor-producing neurons in the rat activated by interleukin-1. Science Wash. DC238: 524-526,1987.
  9. BERNTON, E. W., J. E. BEACH, J. W. HOLADAY, R. C. SMALLRIDGE, and H. G. FEIN. Release of multiple hormones by a direct action of interleukin-1 on pituitary cells. Science Wash. DC 238: 519-521,1987.
  10. BESEDOVSKY, H. 0., A. DEL REY, and E. SORKIN. Lymphokine containing supernatants from GonA stimu­lated cells increase corticosterone blood levels. J. Im­munol 126: 385-387,1981.
  11. BESEDOVSKY, H. 0., A. DEL REY, E. SORKIN, and C. DINARELLO. Immunoregulatory feedback between in­terleukin-1 and glucocorticoid hormones. Science Wash. 1X7233:652-654,1986.
  12. BESEDOVSKY, H. 0., AND E. SORKIN. Network of im-mune-neuroendocrine interactions. Clin. Exp. Immunol 27:1-12,1977.
  13. BESEDOVSKY, H. O., E. SORKIN, M. KELLER, AND J. MULLER. Changes in blood hormone levels during the immune response. Proc Soc Exp. BioL Med. 150:466-470, 1975.
  14. ALOCK, J. E. The immune system as a sensory organ. J. Immunol 132:1067-1070,1984.
  15. BLALOCK, J. E. Relationships between neuroendocrine hormones and lymphokines. In: Lymphokines, edited by E. Pick. Orlando, FL: Academic, 1984, vol. 9, p. 1-13.
  16. BLALOCK, J. E., and C. HARP. Interferon and adreno-corticotropic hormone induction of steroidogenesis, me-lanogenesis, and antiviral activity. Arch. Virol 67:45-49, 1981.
  17. BLALOCK, J. E., H. M. JOHNSON, E. M. SMITH, AND B. A. TORRES. Enhancement of the in vitro antibody re­sponse by thyrotropin. Biochem. Biophys. Res. Commun. 125: 30-34,1985.
  18. BLALOCK, J. E., and E. M. SMITH. Human leukocyte interferon: structural and biological relatedness to adrenocorticotropic hormone and endorphins. Proc. NatL Acad. Sci USA 77: 5972-5974,1980.
  19. BLALOCK, J. E., and E. M. SMITH. Human leukocyte interferon (HuIFN-a): potent endorphin-like opioid ac­tivity. Biochem. Biophys. Res. Commun. 101: 472-478, 1981.
  20. BLALOCK, J. E., AND E. M. SMITH. A complete regula­tory loop between the immune and neuroendocrine sys­tems. Federation Proc. 44:108-111,1985.
  21. BLALOCK, J. E., AND J. D. STANTON. Common path­ways of interferon and hormonal action. Nature Lond. 283: 406-408,1980.
  22. BOHS, C. T., J. C. FISH, T. H. MILLER, AND D. L. TRABER. Pulmonary vascular response to endotoxin in normal and lymphocyte depleted sheep. Circ Shock 6: 13-21,1979.
  23. BOST, K., and J. E. BLALOCK. Molecular characteriza­tion of a corticotropin (ACTH) receptor. MoL Cell En-doer. 44:1-9,1985.
  24. BOST, K. L., E. M. SMITH, AND J. E. BLALOCK. Similar­ity between the corticotropin (ACTH) receptor and a peptide encoded by an RNA that is complementary to ACTH mRNA. Proa Nail Acad. Sci USA 82:1372-1375, 1985.
  25. BOST, K. L., E. M. SMITH, L. B. WEAR, and J. E. BLA­LOCK. Presence of ACTH and its receptor on a B lym-phocytic cell line: a possible autocrine function for a neu-
  26. roendocrine hormone. J. Bid Regul Homeostatic Agents 1: 23-27,1987.
  27. 27.  BROOKS, K. H., J. W. UHR, and E. S. VITETTA. A B cell growth factor-like activity is secreted by cloned neoplas-tic B cells. J. Immunol 133: 3133-3137,1984.
  28. 28.  BROWN, S. L., L. R. SMITH, and J. E. BLALOCK. In-terleukin 1 and interleukin 2 enhance proopiomelanocor-tin gene expression in pituitary cells. J. Immunol 139: 3181-3183,1987.
  29. 29.  BROWN, S. L., S. TOKUDA, L. C. SALAND, and D. E. VAN EPPS. Opioid peptide effects on leukocyte migra­tion. In: Enkephalins and Endorphins. Stress and the Im­mune Response, edited by N. P. Plotnikoff, R. E. Faith, A. J. Murgo, and R. A. Good. New York: Plenum, 1986, p. 367-386.
  30. 30.  BROWN, S. L., and D. E. VAN EPPS. Suppression of T lymphocyte chemotactic factor production by the opioid peptides beta-endorphin and met-enkephalin. J. Im­munol 134: 3384-3390,1985.
  31. 31.  BROWN, S. L., and D. E. VAN EPPS. Opioid peptides modulate production of interferon 7 by human mononu-clear cells. Cell Immunol 103:19-26,1986.
  32. 32.  CALOGERO, A. E., T. LUGER, W. T. GALLUCCI, P. W. GOLD, AND G. P. CHROUSOS. Interleukin 1 and inter­leukin 2 stimulate hypothalamic corticotropin releasing hormone but not pituitary ACTH secretion in vitro (Ab­stract). Proc Annu. Meet Endocrine Soc 69th Indianap­olis 1987, p. 272.
  33. 33.  CARR, D. B., R. BERGLAND, A. HAMILTON, H. BLUME, N. KASTING, M. ARNOLD, M. B. MARTIN, AND M. ROSENBLATT. Endotoxin stimulated opioid peptide secretion: two secretory pools and feedback con­trol in vivo. Science Wash. DC 217: 845-848,1982.
  34. 34.  CARR, D. J. Molecular Characterization of Opiate Recep­tors on Neural and Immune Tissues (PhD thesis). Gal-veston: Univ. of Texas Medical Branch, 1987.
  35. 35.  CARR, D. J. J., K. L. BOST, and J. E. BLALOCK. An antibody to a peptide specified by a RNA that is comple­mentary to 7-endorphin mRNA recognizes an opiate re­ceptor. J. Neuroimmunol 12:329-337,1986.
  36. 36.  CARR, D. J. J., and G. R. KLIMPEL. Enhancement of the generation of cytotoxic T cells by endogenous opiates. J. Neuroimmunol 12: 75-87,1986.
  37. 37.  CLARK, D. A. Immunoregulation of host versus graft responses in the uterus. Immunol Today 5:111-115,1984.
  38. 38.  COHEN, J. J., AND L. S. CRNIC. Glucocorticoids, stress and the immune response. In: Immunopharmacology and the Regulation of Leukocyte Function, edited by D. R. Webb. New York: Dekker, 1982, p. 61-91.
  39. 39.  CUPPS, T. R., AND A. S. FAUCI. Corticosteroid-mediated immunoregulation in man. Immunol Rev. 65: 133-155, 1982.
  40. 40.  CUTZ, E., W. CHAN, N. TRACK, A. GOTH, and S. SAID. Release of vasoactive intestinal peptide in mast cells by histamine liberators. Nature Lond. 275: 661-662,1978.
  41. 41.  DAFNY, N., AND C. REYES-VASQUEZ. Three different types of alpha-interferons alter naloxone-induced absti­nence in morphine addicted rats. Immunopharmacology 9:13-17,1985.
  42. 42.  DANEK, A., M. S. O’DORISIO, T. M. O’DORISIO, and J. M. GEORGE. Specific binding sites for vasoactive in­testinal polypeptide on nonadherent peripheral blood lymphocytes. J. Immunol 131:1173-1177,1983.
  43. 43.  DINARELLO, C. A. Interleukin-1 and the pathogenesis of the acute-phase response. N. Engl. J. Med. 311: 1413-1418,1984.
  44. 44.  DONAHOE, R. M., J. J. MADDEN, F. HOLLINGS-
  45. 30
  47. Volume 69
  49. WORTH, D. SHAFER, and A. FALEK. Morphine de­pression of T cell E-rosetting: definition of the process. Federation Proa 44: 95-99,1985.
  50. 45.  DUNN, A. J., M. L. POWELL, and J. M. GASKIN. Virus-induced increases in plasma corticosterone. Science Wash, DC 238:1423-1424,1987.
  51. 46.  DUPONT, A. G., G. SOMERS, A. C. VAN STEVI-TEGHEM, F. WARSON, and L. VANHAELST. Ectopic adrenocorticotropin production: disappearance after re­moval of inflammatory tissue. J. Clin. Endocrinol. Metab. 58: 654-658,1984.
  52. 47.  ENDO, Y., T. SAKATA, and S. WATANABE. Identifi­cation of proopiomelanocortin-producing cells in the rat pyloric antrum and duodenum by in situ mRNA-cDNA hybridization. Biomed. Res. 6: 253-256,1985.
  53. 48.  FAITH, R. E., H. J. LIANG, A. J. MURGO, and N. P. PLOTNIKOFF. Neuroimmunomodulation with enkepha-lins: enhancement of human natural killer (NK) cell ac­tivity in vitro. Clin. Immunol ImmunopathoL 31:412-418, 1984.
  54. 49.  FARRAR, W. L. Endorphin modulation of lymphokine activity. In: Opioid Peptides in the Periphery, edited by F. Fraioli, A. Isidori, and M. Mazzetti. Amsterdam: Else-vier, 1984, p. 159-165.
  55. 50.  FEHM, H. L., R. HOLL, E. SPATH-SCHWALBE, K. H. VOIGT, and J. BORN. Ability of human corticotropin releasing factor (hCRF) to stimulate cortisol secretion independent from pituitary ACTH. Life Sci 42: 679-686, 1988.
  56. 51.  FONTANA, A., F. KRISTENSEN, R. DUBS, D. GEMSA, and E. WEBER. Production of prostaglandin E and in-terleukin-1 like factor by cultured astrocytes and C6 glioma cells. J. Immunol 129: 2413-2419,1982.
  57. 52.  FONTANA, A., E. WEBER, and J.-M. DAYER. Synthe­sis of interleukin 1/endogenous pyrogen in the brain of endotoxin treated mice: a step in fever induction? J. Im­munol 133:1696-1698,1984.
  59. 53.  FREI, K., S. BODMER, C. SCHWERDEL, and A. FON­TANA. Astrocytes of the brain synthesize interleukin 3-like factors. J. Immunol 135: 4044-4047,1985.
  60. 54.  FROELICH, C. J., and A. D. BANKHURST. The effect of beta endorphin on natural cytotoxicity and antibody de­pendent cellular cytotoxicity. Life Sci 35: 261-265,1984.
  61. 55.  FUCHS, T., L. HAMMARSTROM, C. I. SMITH, AND J. BRUNDIN. Sex dependent induction of human suppres­sor T cells by chorionic gonadotropin. J. Reprod. Im­munol 4:185-190,1982.
  62. 56.  FUKATA, J., AND T. USUI. Effects of recombinant in­terleukin 1-a and p on ACTH levels in mouse pituitary tumor cell line AtT20 (Abstract). Proa Annu. Meet En­docrine Soa 69th Indianapolis 1987, p. 143.
  63. 57.  GEENEN, V., J.-J. LEGROS, P. FRANCHIMONT, M. BAUDRIHAYE, M.-P. DEFRESNE, and J. BONEVER. The neuroendocrine thymus: coexistence of oxytocin and neurophysin in the human thymus. Science Wash. DC 232: 508-511,1986.
  64. 58.  GIACHETTI, A., A. GOTH, and S. I. SAID. Vasoactive intestinal polypeptide (VIP) in rabbit platelets, and rat mast cells (Abstract). Federation Proa 37: 657,1978.
  65. 59.  GILMAN, S. C, J. M. SCHWARTZ, R. J. MILNER, F. E. BLOOM, and J. D. FELDMAN. 0-Endorphin enhances lymphocyte proliferative responses. Proa Natl Acad, Sci USA 79: 4226-4230,1982.
  66. 60.  GOETZL, E. J., T. CHERNOV, F. REYNOLD, and D. G. PAYAN. Neuropeptide regulatidn of the expression of immediate hypersensitivity. J. Immunol 135, Suppl 2: 802s-805s, 1985.
  68. 61.  GOETZL, E. J., T. CHERNOV-ROGAN, M. P. COOKE, F. RENOLD, and D. G. PAYAN. Endogenous somatosta-tin-like peptides of rat basophilic leukemic cells. J. Im­munol 135: 2707-2712,1985.
  69. 62.  HALL, N. R., J. P. McGILLIS, B. L. SPANGELO, and A. L. GOLDSTEIN. Evidence that thymosins and other biologic response modifiers can function as neuroactive immunotransmitters. J. Immunol. 135, Suppl. 2: 806s-811s, 1985.
  70. 63.  HANNAPPEL, E., G.-J. XU, J. MORGAN, J. HEMP-STEAD, and B. L. HORECKER. Thymosin beta four: a ubiquitous peptide in rat and mouse tissues. Proa Natl Acad. Sci USA 79: 2172-2175,1981.
  71. 64.  HARBOUR, D. V., E. M. SMITH, and J. E. BLALOCK. A novel processing pathway for proopiomelanocortin in lymphocytes: endotoxin induction of a new prohormone-cleaning enzyme. J. Neurosci Res. 18: 95-101,1987.
  72. 65.  HARBOUR, D. V., E. M. SMITH, AND W. J. MEYER. MOLT 4 T lymphoblastic leukemia cell line produces im-munoreactive thyroid stimulating hormone (ir-TSH) (Abstract). Proa Annu. Meet. Endocrine Soa 69th In­dianapolis 1987, p. 181.
  73. 66.  HARBOUR-McMENAMIN, D. V., E. M. SMITH, and J. E. BLALOCK. Endotoxin induction of leukocyte-de­rived proopiomelanocortin related peptides. Infect Immun. 48: 813-819,1984.
  74. 67.  HARBOUR-McMENAMIN, D. V., E. M. SMITH, AND J. E. BLALOCK. Production of lymphocyte derived cho­rionic gonadotropin in a mixed lymphocyte reaction. Proa Natl Acad. Sci USA 83: 6834-6838,1986.
  75. 68.  HAZUM, E. K., K. CHANG, and P. CUATRECASAS. Specific non opiate receptors for 0-endorphin. Science Wash DC 205:1033-1035,1979.
  76. 69.  HEIJNEN, C. J., and R. E. BALLIEUX. Influence of opioid peptides on the immune system. Inst Adv. Health. Sci 3:114-117,1986.
  77. 70.  HEIJNEN, C. J., C. BEVERS, A. KAVELAARS, and R. E. BALLIEUX. Effect of a-endorphin on the antigen-induced primary antibody response of human blood B cells in vitro. J. Immunol 136: 213-216,1986.
  78. 71.  HIESTAND, P. C, P. MEKLER, R. NORDMANN, A. GRIEDER, and C. PERMMONGKOL. Prolactin as a modulator of lymphocyte responsiveness provides a pos­sible mechanism of action for cyclosporin. Proa Natl Acad, Sci USA 83: 2599-2603,1986.
  79. 72.  JANKOVIC, B. D., and K. ISAKOVIC. Neuroendocrine correlates of immune response. Int Arch, Allergy Appl Immunol 45: 360-384,1973.
  81. 73.  JOHNSON, H. M., E. M. SMITH, B. A. TORRES, and J. E. BLALOCK. Neuroendocrine hormone regulation of in vitro antibody production. Proa Natl Acad, Sci USA 79: 4171-4174,1982.
  82. 74.  JOHNSON, H. M., and B. A. TORRES. Regulation of lymphokine production by arginine vasopressin and oxy­tocin: modulation of lymphocyte function by neurohypo-physeal hormones. J. Immunol 135, Suppl 2: 773s-775s, 1985.
  83. 75.  JOHNSON, H. M., B. A. TORRES, E. M. SMITH, L. D. DION, and J. E. BLALOCK. Regulation of lymphokine (interferon-7) production by corticotropin. J. Immunol 132: 246-250,1984.
  84. 76.  KAY, N., J. ALLEN, and J. E. MORLEY. Endorphins stimulate normal human peripheral blood lymphocyte natural killer activity. Life Sci 35: 53-59,1984.



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