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Serum and acute phase protein modulation of the effector phase of lymphokine‐activated killer cells
Author(s) -
Dayman Gary L.,
Taylor Dorothy L.,
Liu Frank J.,
Lavedan Pierre,
Savage Howard E.,
Schantz Stimson P.
Publication year - 1993
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1288/00005537-199303000-00010
Subject(s) - lymphokine activated killer cell , effector , lymphokine , immunology , k562 cells , interleukin 2 , cancer research , medicine , biology , immune system , t cell , interleukin 21 , leukemia
An understanding of the role that immunomodulatory factors play in the effector phase of lymphokine‐activated killer (LAK) activity is essential for the development of biologic response modifiers for use in the treatment of advanced carcinoma. Fifteen head and neck cancer patients were studied. Single‐donor killer cells activated by recombinant interleukin‐2 (10 U/mL) and induced in either a complete medium or complete medium plus a 10% autologous serum solution were used. Effector phase solutions of 25% autologous serum were used in chromium 51 release assays to determine sera immunomodulation of LAK cell cytotoxicity. Both K562 and squamous carcinoma (MDA686‐Ln) tumor cell lines were tested. Significant effector phase inhibition (EPI) of cytotoxicity occurred in 40% of studied patients. Seventy percent of patients with stage III or IV or recurrent disease exhibited EPI, whereas only 20% of patients with stage I or II disease and 30% of controls did so. EPI of cancer patient serum correlated directly with α 1 ‐antitrypsin, α 1 ‐acid glycoprotein, and C‐reactive protein (CRP) levels (MDA686‐Ln targets) ( r = 0.6, 0.7, and 0.6, respectively) ( P <.02). Neither EPI against K562 targets nor EPI in control patients correlated with acute phase protein levels. These findings suggest that advances in in vivo immunomodulatory therapy will be dependent upon further elucidation of serologic inhibition of the effector phase of the LAK cell phenomenon. The relationship between LAK cell recognition and EPI requires further investigation.