Natural killer cells in intravenous drug abusers with lymphadenopathy syndrome

G. Poli, M. Introna, F. Zanaboni, G. Peri, M. Carbonari, F. Aiuti, A. Lazzarin, M. Moroni, A. Mantovani

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

We have investigated 25 intravenous drug abusers with the clinical and laboratory features of lymphadenopathy syndrome (LAS) and 10 AIDS patients for the expression of NK activity. LAS and AIDS patients had low NK cytotoxicity compared to normal donors. The defective NK cytotoxicity was analysed in the eight LAS subjects with most marked depression. NK effectors were identified by morphology (large granular lymphocytes, LGL) and monoclonal antibody-defined surface markers (B73.1, N901, HNK1). LAS patients had normal percentages of LGL and B73.1+ and N901+ cells, with the exception of two subjects with very low frequency of B73.1+ and N901+ cells. The percentage of HNK1+ cells was increased in LAS, probably because of the reactivity of this reagent with a subset of conventional OKT8+ cells, relatively augmented in LAS subjects. Depletion of monocytes did not enhance NK activity consistently. LAS patients had a normal frequency of cells capable of binding K562. In-vitro exposure to interferon beta (natural) or gamma (recombinant) augmented the defective NK activity of LAS subjects. Thus, patients with LAS have defective NK activity that cannot be accounted for by a low frequency of the relevant effector cells or by monocytic suppressors. These observations suggest a functional defect of NK cells at one or more of the post-binding steps required for the completion of killing.

Original languageEnglish
Pages (from-to)128-135
Number of pages8
JournalClinical and Experimental Immunology
Volume62
Issue number1
Publication statusPublished - 1985

Fingerprint

AIDS-Related Complex
Drug Users
Natural Killer Cells
Acquired Immunodeficiency Syndrome
Lymphocytes
Interferon-beta
Interferon-gamma
Monocytes
Monoclonal Antibodies
Tissue Donors

ASJC Scopus subject areas

  • Immunology

Cite this

Natural killer cells in intravenous drug abusers with lymphadenopathy syndrome. / Poli, G.; Introna, M.; Zanaboni, F.; Peri, G.; Carbonari, M.; Aiuti, F.; Lazzarin, A.; Moroni, M.; Mantovani, A.

In: Clinical and Experimental Immunology, Vol. 62, No. 1, 1985, p. 128-135.

Research output: Contribution to journalArticle

Poli, G, Introna, M, Zanaboni, F, Peri, G, Carbonari, M, Aiuti, F, Lazzarin, A, Moroni, M & Mantovani, A 1985, 'Natural killer cells in intravenous drug abusers with lymphadenopathy syndrome', Clinical and Experimental Immunology, vol. 62, no. 1, pp. 128-135.
Poli G, Introna M, Zanaboni F, Peri G, Carbonari M, Aiuti F et al. Natural killer cells in intravenous drug abusers with lymphadenopathy syndrome. Clinical and Experimental Immunology. 1985;62(1):128-135.
Poli, G. ; Introna, M. ; Zanaboni, F. ; Peri, G. ; Carbonari, M. ; Aiuti, F. ; Lazzarin, A. ; Moroni, M. ; Mantovani, A. / Natural killer cells in intravenous drug abusers with lymphadenopathy syndrome. In: Clinical and Experimental Immunology. 1985 ; Vol. 62, No. 1. pp. 128-135.
@article{59c7154b7c3747828cbbd10d639cab9c,
title = "Natural killer cells in intravenous drug abusers with lymphadenopathy syndrome",
abstract = "We have investigated 25 intravenous drug abusers with the clinical and laboratory features of lymphadenopathy syndrome (LAS) and 10 AIDS patients for the expression of NK activity. LAS and AIDS patients had low NK cytotoxicity compared to normal donors. The defective NK cytotoxicity was analysed in the eight LAS subjects with most marked depression. NK effectors were identified by morphology (large granular lymphocytes, LGL) and monoclonal antibody-defined surface markers (B73.1, N901, HNK1). LAS patients had normal percentages of LGL and B73.1+ and N901+ cells, with the exception of two subjects with very low frequency of B73.1+ and N901+ cells. The percentage of HNK1+ cells was increased in LAS, probably because of the reactivity of this reagent with a subset of conventional OKT8+ cells, relatively augmented in LAS subjects. Depletion of monocytes did not enhance NK activity consistently. LAS patients had a normal frequency of cells capable of binding K562. In-vitro exposure to interferon beta (natural) or gamma (recombinant) augmented the defective NK activity of LAS subjects. Thus, patients with LAS have defective NK activity that cannot be accounted for by a low frequency of the relevant effector cells or by monocytic suppressors. These observations suggest a functional defect of NK cells at one or more of the post-binding steps required for the completion of killing.",
author = "G. Poli and M. Introna and F. Zanaboni and G. Peri and M. Carbonari and F. Aiuti and A. Lazzarin and M. Moroni and A. Mantovani",
year = "1985",
language = "English",
volume = "62",
pages = "128--135",
journal = "Clinical and Experimental Immunology",
issn = "0009-9104",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - Natural killer cells in intravenous drug abusers with lymphadenopathy syndrome

AU - Poli, G.

AU - Introna, M.

AU - Zanaboni, F.

AU - Peri, G.

AU - Carbonari, M.

AU - Aiuti, F.

AU - Lazzarin, A.

AU - Moroni, M.

AU - Mantovani, A.

PY - 1985

Y1 - 1985

N2 - We have investigated 25 intravenous drug abusers with the clinical and laboratory features of lymphadenopathy syndrome (LAS) and 10 AIDS patients for the expression of NK activity. LAS and AIDS patients had low NK cytotoxicity compared to normal donors. The defective NK cytotoxicity was analysed in the eight LAS subjects with most marked depression. NK effectors were identified by morphology (large granular lymphocytes, LGL) and monoclonal antibody-defined surface markers (B73.1, N901, HNK1). LAS patients had normal percentages of LGL and B73.1+ and N901+ cells, with the exception of two subjects with very low frequency of B73.1+ and N901+ cells. The percentage of HNK1+ cells was increased in LAS, probably because of the reactivity of this reagent with a subset of conventional OKT8+ cells, relatively augmented in LAS subjects. Depletion of monocytes did not enhance NK activity consistently. LAS patients had a normal frequency of cells capable of binding K562. In-vitro exposure to interferon beta (natural) or gamma (recombinant) augmented the defective NK activity of LAS subjects. Thus, patients with LAS have defective NK activity that cannot be accounted for by a low frequency of the relevant effector cells or by monocytic suppressors. These observations suggest a functional defect of NK cells at one or more of the post-binding steps required for the completion of killing.

AB - We have investigated 25 intravenous drug abusers with the clinical and laboratory features of lymphadenopathy syndrome (LAS) and 10 AIDS patients for the expression of NK activity. LAS and AIDS patients had low NK cytotoxicity compared to normal donors. The defective NK cytotoxicity was analysed in the eight LAS subjects with most marked depression. NK effectors were identified by morphology (large granular lymphocytes, LGL) and monoclonal antibody-defined surface markers (B73.1, N901, HNK1). LAS patients had normal percentages of LGL and B73.1+ and N901+ cells, with the exception of two subjects with very low frequency of B73.1+ and N901+ cells. The percentage of HNK1+ cells was increased in LAS, probably because of the reactivity of this reagent with a subset of conventional OKT8+ cells, relatively augmented in LAS subjects. Depletion of monocytes did not enhance NK activity consistently. LAS patients had a normal frequency of cells capable of binding K562. In-vitro exposure to interferon beta (natural) or gamma (recombinant) augmented the defective NK activity of LAS subjects. Thus, patients with LAS have defective NK activity that cannot be accounted for by a low frequency of the relevant effector cells or by monocytic suppressors. These observations suggest a functional defect of NK cells at one or more of the post-binding steps required for the completion of killing.

UR - http://www.scopus.com/inward/record.url?scp=0021925522&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021925522&partnerID=8YFLogxK

M3 - Article

C2 - 2415279

AN - SCOPUS:0021925522

VL - 62

SP - 128

EP - 135

JO - Clinical and Experimental Immunology

JF - Clinical and Experimental Immunology

SN - 0009-9104

IS - 1

ER -