Ligation of ICAM-1 Molecules Inhibits Target Cell-Induced Granule Exocytosis of IL-12-Activated Natural Killer Cells

Cho, D H; Song, Han-Jung; Kang, Hyung Sik; Yoon, Suk Ran; Lee, Hee Gu; Pyun, Kwang Ho; Lee, W J; Kim, Y B; Choi, In Pyo

doi:10.1006/cimm.1999.1592

Cited by 14 publications

(11 citation statements)

References 39 publications

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“…Because perforin KO LAK cells have impaired cytolytic function, 14 the cytolytic ability of LAK cells stimulated by anti-NK1.1 antibody-coated plates was measured indirectly by using the BLT esterase assay to detect granzyme secretion. 11 Consistent with previous reports, 5 WT LAK cells have decreased esterase release in the presence of anti-2B4 or anti-CD48 blocking antibodies (Figure 2A). In contrast, perforin KO LAK cells do not exhibit a decrease in esterase activity in the presence of anti-2B4 or anti-CD48 blocking antibodies (Figure 2A).…”

Section: Wt Lak Targetssupporting

confidence: 92%

“…Coated plates were used to stimulate 3 ϫ 10 5 LAK cells per well in the presence of 10 g/mL 2.4G2 mAb with or without 10 g/mL ␣CD48 mAb or ␣2B4 mAb. After 6 hours of incubation at 37°, 50 L supernatant was analyzed from triplicate samples for N-␣-benzyloxycarbonyl-Llysine thiobenzyl (BLT) esterase activity as previously described by Cho et al 11 The % specific esterase release ϭ (experimental esterase release Ϫ spontaneous release)/(maximum release with Triton X Ϫ spontaneous release).…”

Section: Blt Ester Assaymentioning

confidence: 99%

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2B4 inhibits NK-cell fratricide

Taniguchi

Guzior

Kumar

2007

Blood

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Section: Wt Lak Targetssupporting

confidence: 92%

Section: Blt Ester Assaymentioning

confidence: 99%

2B4 inhibits NK-cell fratricide

Taniguchi

Guzior

Kumar

2007

Blood

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“…In contrast, the soluble form of ICAM-1 (sICAM-1) is elevated in breast cancer (Klein et al, 1995;Merendino et al, 2001;O'Hanlon et al, 2002) and is predictive of poorer response to chemotherapy and poorer prognosis (O'Hanlon et al, 2002;Zhang and Adachi, 1999). sICAM-1 reflects generalized inflammation (Blann et al, 2002) and exerts immunomodulatory effects such as suppression of natural killer cell and T-cell function and inhibition of leukocyte binding to target cells, including formation of natural killer cell/tumor cell conjugates (Cho et al, 2000;Kaihara et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Predictors of inflammation in response to anthracycline-based chemotherapy for breast cancer

Mills

Ancoli‐Israel

Parker

et al. 2008

Brain, Behavior, and Immunity

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Although chemotherapy for breast cancer can increase inflammation, few studies have examined predictors of this phenomenon. This study examined potential contributions of demographics, disease characteristics, and treatment regimens to markers of inflammation in response to chemotherapy for breast cancer. Thirty-five women with stage I -III-A breast cancer (mean age 50 years) were studied prior to cycle 1 and prior to cycle 4 of anthracycline-based chemotherapy. Circulating levels of inflammatory markers with high relevance to breast cancer were examined, including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), Interleukin-1 receptor antagonist (IL1-RA), vascular endothelial growth factor (VEGF), soluble intercellular adhesion molecule-1 (sICAM-1), Interleukin-(IL-6), soluble P-selectin (sP-selectin), and von Willebrand factor (vWf). Chemotherapy was associated with elevations in VEGF (p≤0.01), sICAM-1 (p≤0.01), sP-selectin (p≤0.02) and vWf (p≤0.05). Multiple regression analysis controlling for age and body mass index (BMI) showed that higher post-chemotherapy levels of inflammation were consistently related to higher prechemotherapy levels of inflammation (p's ≤0.05) as well as to certain disease characteristics. Postchemotherapy IL-6 levels were higher in patients who had larger tumors (p≤0.05) while postchemotherapy VEGF levels were higher in patients who had smaller tumors (p≤0.05). Postchemotherapy sP-selectin levels were highest in women who had received epirubicin, cytoxan, 5fluorouracil chemotherapy (p≤0.01). These findings indicate that chemotherapy treatment can be associated with elevations in certain markers of inflammation, particularly markers of endothelial and platelet activation. Inflammation in response to chemotherapy is most significantly related to inflammation that existed prior to chemotherapy but also potentially to treatment regimen and to certain disease characteristics.

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“…In addition to increasing signal transduction, adhesion molecules participate in conjugate formation to affect the immune response [39]. The increased adhesion ability of NK cells increases their powerful conjugation ability to target cells.…”

Section: Discussionmentioning

confidence: 99%