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PubMed2003

Interferon-beta prevents cytokine-induced neutrophil infiltration and attenuates blood-brain barrier disruption.

Inflammation can contribute to brain injury, such as that resulting from ischemia or trauma. The authors have previously shown that the cytokine interferon-beta (IFN-beta) affords protection against ischemic brain injury, which was associated with a diminished infiltration of neutrophils and a reduction in blood-brain barrier (BBB) disruption. The goal of the current study was to directly assess the effects of IFN-beta on neutrophil infiltration, with the use of an in vivo assay of neutrophil infiltration with relevance to ischemic brain injury. Intrastriatal injection of recombinant rat cytokine-induced neutrophil chemoattractant-1, a member of the interleukin-8 family (1 microg in 1 microl), triggered massive infiltration of neutrophils and extensive BBB disruption 6 hours later, as measured using immunofluorescence microscopy and magnetic resonance imaging in the rat, respectively. Depleting the animals of neutrophils before interleukin-8 injection prevented BBB disruption. Treatment with IFN-beta (5 x 106 U/kg) almost completely prevented neutrophil infiltration and attenuated BBB damage. Gelatinase zymography showed matrix metalloproteinase-9 expression in the ipsilateral striatum after interleukin-8 injection. Both neutrophil depletion and IFN-beta treatment downregulated matrix metalloproteinase-9. IFN-beta has already been approved for human use as a treatment for the chronic inflammatory disorder multiple sclerosis. The potential value of IFN-beta as a treatment that can attenuate acute brain inflammation is considered.

Animals↗

PubMed2005

'Specific' cutaneous infiltrate of B-cell chronic lymphocytic leukemia at the site of a florid herpes simplex infection.

BACKGROUND: Specific cutaneous infiltrates in patients with leukemia generally carry a grim prognosis. However, non-neoplastic skin diseases may be associated with recruitment of normal and neoplastic leukocytes circulating in the peripheral blood. In those instances, neoplastic cells may be detected in skin lesions without an adverse effect on prognosis. METHODS: In a patient with B-cell chronic lymphocytic leukemia, a specific infiltrate developed at the site of a florid herpes simplex infection. Clinically, the lesion presented itself as an ulcerated tumor. RESULTS: Histopathologically, the lesion was characterized by a dense, diffuse infiltrate of small hyperchromatic lymphocytes throughout the entire dermis. Lymphocytes showed an aberrant CD20(+)/CD43(+)/CD5(+) phenotype of neoplastic B cells, and monoclonal rearrangement of immunoglobulin gamma genes could be demonstrated by polymerase chain reaction. Although criteria for leukemia cutis were fulfilled, the patient did well. CONCLUSIONS: The cutaneous infiltrate of neoplastic cells seemed to be part of a physiologic response to the antigenic stimulus, rather than indicating an exacerbation of leukemia. Ziemer M, Bornkessel A, Hahnfeld S, Weyers W. 'Specific' cutaneous infiltrate of B-cell chronic lymphocytic leukemia at the site of a florid herpes simplex infection.

Aged↗

PubMed1992

Immunohistochemical characterization of cellular infiltrates in squamous cell carcinoma and Bowen's disease occurring in one patient.

We investigated populations of the infiltrating cells in Bowen's disease (BD) and squamous cell carcinoma (SCC), both of which arose in the same patient, using the Avidin-Biotin-peroxidase complex method with eight monoclonal antibodies. T lymphocytes were most predominant among infiltrating cells; NK cells, B cells, and monocytes were rarely seen in either BD or SCC. Analysis of subsets of the infiltrating T lymphocytes revealed that the number of suppressor/cytotoxic (s/c) T cells was twice that of helper/inducer (h/i) T cells in BD, while the number of s/c T cells was lower than that of h/i T cells in SCC. The immunohistochemical results in the present case differed from those of predominant infiltration of h/i T cells and of s/c T cells in three other reports of BD and SCC. These results suggest that the population of the cellular infiltrates may be modulated by the nature of tumors and by the immuno-competent state of the hosts.

Aged↗

PubMed2000

Correlation between deposition of immuno-components and infiltration pattern of polymorphonuclear leukocytes in the lesions of chronic urticaria.

Urticaria is often associated with perivascular infiltration of leukocytes into the lesions. Although mast cell-derived chemical mediators are considered to play crucial roles in the infiltration of leukocytes as well as in the dermal edema, other mechanisms for the leukocyte infiltration have not been well defined. This study revealed that approximately 25% of the cases of chronic idiopathic urticaria in whom wheals had continued for more than 12 h had deposition of immuno-components in the lesions, although histological examination of the lesions did not show leukocytoclastic vasculitis. In these lesions with deposition of immuno-components, both neutrophils and eosinophils had infiltrated at a constant ratio (approximately 2:1), whereas, in the lesions without deposition, a variable population of leukocytes was seen. This result suggests that activation of complements occurs in the lesions of a considerable percentage of patients with chronic idiopathic urticaria and that the complement fragments influence the infiltration patterns of polymorphonuclear leukocytes.

Adult↗

PubMed1992

Image analysis of stage 1 melanoma (1.00-2.50 mm): lymphocytic infiltrates related to metastasis and survival.

Image analysis of histologic sections of 11 patients with clinical Stage 1 melanoma, 1.00 mm-2.50 mm, who developed metastasis, was done to determine the significance of lymphocytic infiltrates relative to metastasis and survival. An age, sex, site, and thickness matched control group of non-metastasizing clinical Stage 1 melanoma revealed no significant difference in the lymphocytic infiltrate parameters from the metastasizing group with the exception of the ratio of lymphocyte infiltrate width to the tumor width (p = 0.003). Increased lymphocytic infiltrates within the tumor and subjacent to its base significantly correlated with delayed time to metastasis (p = 0.014 and p < 0.001, respectively) and longer survival period (p = 0.045 and p < 0.001, respectively). Lymphocytic infiltrate area at the tumor base in relation to tumor area was of prognostic value: the larger the ratio, the greater the time interval from metastasis to death (p = 0.008).

Humans↗

PubMed2006

Cytotoxic markers and frequency predict functional capacity of natural killer cells infiltrating renal cell carcinoma.

PURPOSE: Renal cell carcinoma harbors high numbers of infiltrating lymphocytes with apparent limited efficacy in tumor control. This study focused on the natural killer (NK) cells infiltrating renal cell carcinoma. EXPERIMENTAL DESIGN: Tumor-infiltrating lymphocytes (TIL) were isolated from renal cell carcinoma and analyzed for NK cell frequency and phenotype (n = 34). NK cells were enriched and tested for effector function. RESULTS: Two renal cell carcinoma subtypes were identified, one containing high (>20% of the lymphocyte population, n = 14), the other low (<20%, n = 20), NK cell numbers. NK cells of both groups were noncytolytic ex vivo but differed in CD16 and cytotoxic effector molecule expression as well as in their capacity to acquire cytotoxic activity: The majority of NK cells from tumors with high NK cell content (high NK-TIL) were CD16(bright), whereas few CD16bright NK cells were found in tumors with low NK cell frequencies (low NK-TIL). The CD16 dichotomy correlated with different capacities to develop cytotoxicity after short-term activation with interleukin-2 ex vivo: Low NK-TIL remained noncytolytic against K562 and unresponsive to signals via the activating receptor NKp46 despite expression of receptor and adaptor molecules. In contrast, high NK-TIL acquired cytotoxic function. As described for peripheral CD16bright NK cells, NK cells from high-NK tumors showed high per cell expression of granzyme A, granzyme B, and perforin. NK cells from low NK-TIL resembled CD16(neg/dim) peripheral NK cells with few cytotoxin+ cells and lower expression of perforin. CONCLUSION: The extent of NK cell infiltration and the expression of markers (CD16 and cytotoxins) predict the functional capacity of NK cells infiltrating renal cell carcinoma and can be used to characterize subgroups of renal cell carcinoma.

Adult↗

PubMed2001

Ischemia-reperfusion of rat myocardium activates nuclear factor-KappaB and induces neutrophil infiltration via lipopolysaccharide-induced CXC chemokine.

BACKGROUND: Mechanisms by which neutrophils are attracted to the myocardium in ischemia/reperfusion are not fully defined. Lipopolysaccharide-induced CXC chemokine (LIX), cytokine-induced neutrophil chemoattractant (KC), and macrophage inflammatory protein-2 (MIP-2) are rodent chemokines with potent neutrophil-chemotactic activity. The goals of the present study were to evaluate the roles of these chemokines in a rat model of ischemia/reperfusion and to examine the mechanisms of chemokine induction by oxidative stress and cytokines in cultured cardiomyocytes. METHODS AND RESULTS: Male Wistar-Kyoto rats underwent 45 minutes of ligation of the left anterior descending coronary artery, followed by reperfusion for various periods. Compared with sham-operated controls, myocardium from reperfused animals had higher levels of free radicals, increased neutrophil infiltration evidenced histologically and by elevated myeloperoxidase activity, and increased nuclear factor (NF)-kappaB DNA binding activity. Ischemia-reperfusion also induced the expression of interleukin-1beta, tumor necrosis factor (TNF)-alpha, LIX, KC, and MIP-2 mRNA and protein. LIX expression was localized to resident myocardial cells, whereas KC and MIP-2 were expressed only in infiltrating inflammatory cells. Neutralization of LIX inhibited 79% of neutrophil infiltration into previously ischemic myocardium. In contrast, neutralization of KC and MIP-2 reduced neutrophil infiltration by only 28% and 37%, respectively. In cultured cardiomyocytes, LIX expression was induced by oxidative stress or TNF-alpha and was blocked by the NF-kappaB inhibitor pyrrolidinedithiocarbamate. CONCLUSIONS: LIX is expressed by resident myocardial cells during ischemia-reperfusion and is induced in cultured cardiomyocytes by oxidative stress or TNF-alpha via NF-kappaB activation. Although KC and MIP-2 are expressed by inflammatory cells infiltrating the myocardium during reperfusion after ischemia, neutrophil recruitment to reperfused rat myocardium is mainly due to cardiomyocyte expression of LIX.

Animals↗

PubMed2005

Primary lung adenocarcinoma with massive lymphocyte infiltration.

We report 6 cases of adenocarcinoma with massive lymphocyte infiltration. This adenocarcinoma is found in 0.7% of surgically resected primary lung adenocarcinomas. The tumor was located in the peripheral portion in all cases. Lymph node metastasis was detected in 4 cases. The mean follow-up period was 49.8 months; all patients were alive without recurrence despite advanced pathologic stage. Histologically, the tumors revealed an acinar and glandular structure, and the cancer epithelium was destroyed by infiltrating lymphocytes. The lung parenchyma was destroyed by the severe inflammatory cell infiltration without dense fibrosis. Immunohistochemical staining revealed that most infiltrating lymphocytes were positive for CD3 or CD20. None of the tumors were positive for latent membrane protein-1, bcl-2, or Epstein-Barr virus-encoded small RNA-1. This type of adenocarcinoma occurs in old age, and good outcome and distinctive histologic features were observed. We refer to it as primary lung adenocarcinoma with massive lymphocyte infiltration.

Adenocarcinoma↗

PubMed2002

A selectin inhibitor decreases neutrophil infiltration during acute Mannheimia haemolytica pneumonia.

The degree to which the selectin inhibitor TBC1269 reduces neutrophil infiltration in specific microscopic locations of the lung during acute pneumonia of neonates was determined. Neonatal calves were inoculated intrabronchially with Mannheimia (Pasteurella) haemolytica or saline, and lung tissue was collected at 2 and 6 hours postinoculation (PI). One 6-hour group inoculated with M. haemolytica received TBC1269 intravenously before and after inoculation with M. haemolytica. Infiltrates of neutrophils were significantly higher in the alveolar lumen and septae but lower in the bronchial lumen and epithelium at 6 hours PI than at 2 hours PI. Significantly fewer neutrophils (P < 0.05) were present in the alveolar lumen and septae, and the bronchiolar lumen and lamina propria in the lungs of TBC1269-treated calves compared with untreated calves at 6 hours PI. TBC1269 did not alter the infiltration into bronchi and blood vessels or the expression of the selectin-independent adhesion molecule, ICAM-1. This work suggests that during acute pneumonia of neonates 1) neutrophil infiltrates progressively increase in the alveolar lumens and septae but decrease in the bronchial lumen and epithelium with time, 2) TBC1269 reduces neutrophil infiltration into specific regions of alveoli and bronchioles rather than uniformly throughout the lung, and 3) selectin inhibition does not affect the location and intensity of ICAM-1 expression.

Animals↗

PubMed2026

Tumour-infiltrating lymphocytes differ across MammaPrint® classifications in breast cancer.

MammaPrint® refines risk stratification in early oestrogen receptor-positive, HER2-negative breast cancer, evolving from a binary to a four-tier classification (UltraLow-Risk, Low-Risk, High-Risk 1, and High-Risk 2). The relationship between routine histopathological features, immune infiltration, and genomic risk within this framework remains incompletely characterized in luminal disease. We retrospectively analysed 492 luminal breast carcinomas with available MammaPrint® results. Clinicopathological variables (including histological subtype, grade, Ki-67, hormone receptor expression, lymphovascular invasion (LVI), and HER2-low status) were recorded. Stromal tumour-infiltrating lymphocytes (TILs) were quantified according to the criteria of Salgado et al. and spatially categorized as immune-deserted, stromal-restricted, immune-excluded, or inflamed patterns. CD4 and CD8 infiltration was assessed by immunohistochemistry on tissue microarrays. Associations with binary and four-tier MammaPrint® categories were examined using multivariable models. High-Risk tumours (41%) were enriched for increased grade, Ki-67, and LVI and lower PR expression. In High-Risk tumours, inflamed spatial patterns were more frequent and median TIL levels were significantly higher compared with Low-Risk tumours (15% vs 5%, P < 0.001). CD4 and CD8 infiltration increased with genomic risk, and CD4 retained a modest but statistically significant association after adjustment for conventional pathological variables. In the four-tier model, UltraLow-Risk/Low-Risk tumours showed minimal TILs and were enriched for invasive lobular carcinoma, whereas High-Risk 1/High-Risk 2 tumours displayed progressively higher proliferative and immune features. No association was observed between HER2-low status and genomic risk. Immune infiltration parallels proliferative and genomic risk gradients in luminal breast cancer. These findings indicate that immune descriptors align with the genomic risk continuum, although their independent prognostic contribution beyond established genomic assays requires further evaluation.

Humans↗

PubMed1999

High incidence of meningeal infiltration by leukemic cells after infection of chimeric virus between neuropathogenic and non-neuropathogenic retroviruses.

Friend murine leukemia virus (F-MuLV) clone A8, previously shown to cause spongiform degeneration in rat brain, induced leukemia within 10 weeks after infection when inoculated into newborn rats. The chimeric virus Rec2, which contains the pol and env genes of 57 virus on the background of A8 and does not cause spongiform degeneration in the central nervous system (CNS), induced leukemic cell infiltration of the CNS, mainly of the meningeal region, in 58.3% of infected rats. In contrast, A8 induced little or no leukemic cell infiltration of the CNS. Other chimeric viruses containing the LTR and the 5' half of the 5' leader sequence of A8 induced aggressive leukemia, and after infection of these viruses, leukemic cell infiltration of the CNS was only observed in less than 20.0% of the rats. These results indicate that the fragment containing the LTR and the 5' half of the 5' leader sequence of A8 is essential for induction of aggressive leukemia in rats but is not sufficient to cause CNS infiltration. We found that leukemic cell infiltration of the CNS is dependent on the sequence of the virus.

3T3 Cells↗

PubMed2002

Lack of effector cell function and altered tetramer binding of tumor-infiltrating lymphocytes.

Tumor-specific CD8 T cell responses to MCA102 fibrosarcoma cells expressing the cytotoxic T cell epitope gp33 from lymphocytic choriomeningitis virus were studied. MCA102(gp33) tumors grew progressively in C57BL/6 mice, despite induction of peripheral gp33-tetramer(+) T cells that were capable of mediating antiviral protection, specific cell rejection, and concomitant tumor immunity. MCA102(gp33) tumors were infiltrated with a high number ( approximately 20%) of CD11b(+)CD11c(-) macrophage-phenotype cells that were able to cross-present the gp33 epitope to T cells. Tumor-infiltrating CD8 T cells exhibited a highly activated phenotype but lacked effector cell function. Strikingly, a significant portion of tumor-infiltrating lymphocytes expressed TCRs specific for gp33 but bound MHC tetramers only after cell purification and a 24-h resting period in vitro. The phenomenon of "tetramer-negative T cells" was not restricted to tumor-infiltrating lymphocytes from MCA102(gp33) tumors, but was also observed when Ag-specific T cells derived from an environment with high Ag load were analyzed ex vivo. Thus, using a novel tumor model, allowing us to trace tumor-specific T cells at the single cell level in vivo, we demonstrate that the tumor microenvironment is able to alter the functional activity of T cells infiltrating the tumor mass.

Animals↗

PubMed1998

[Magnetic resonance imaging: more sensitive method in the detection of leukemic central nervous system infiltration].

PURPOSE: To define the ability of magnetic resonance imaging (MRI) in identifying leukemic infiltration of central nervous system (CNS) in children. METHODS: The MRI of CNS was carried out in 54 leukemic children (mean age 8.9 years). The results were compared with CSF cytology and neurological examinations. RESULTS: Leukemic involvement of CNS (1 intracerebral infiltration, 5 meningeal intracranial infiltration, and 5 cases of intraspinal infiltration) was found in 11 children (20.4%)--6 of them were before treatment. Blasts in CSF were found only in 3 examined children. CONCLUSIONS: The results of the study implicate the importance of routine MRI screening in leukemic children. We found especially important to perform the first examination before the onset of treatment because therapy may cause very quick regression of leukemic infiltration in CNS.

Adolescent↗

PubMed2001

Green tea polyphenol (-)-epigallocatechin-3-gallate treatment to mouse skin prevents UVB-induced infiltration of leukocytes, depletion of antigen-presenting cells, and oxidative stress.

Ultraviolet (UV) radiation-induced infiltrating leukocytes, depletion of antigen-presenting cells, and oxidative stress in the skin play an important role in the induction of immune suppression and photocarcinogenesis. Earlier we have shown that topical application of polyphenols from green tea or its major chemopreventive constituent (-)-epigallocatechin-3-gallate (EGCG) prevents UV-B-induced immunosuppression in mice. To define the mechanism of prevention, we found that topical application of EGCG (3 mg/mouse/3 cm(2) of skin area) to C3H/HeN mice before a single dose of UV-B (90 mJ/cm(2)) exposure inhibited UV-B-induced infiltration of leukocytes, specifically the CD11b+ cell type, and myeloperoxidase activity, a marker of tissue infiltration of leukocytes. EGCG treatment was also found to prevent UV-B-induced depletion in the number of antigen-presenting cells when immunohistochemically detected as class II MHC+ Ia+ cells. UV-B-induced infiltrating cell production of H2O2 and nitric oxide (NO) was determined as a marker of oxidative stress. We found that pretreatment of EGCG decreased the number of UV-B-induced increases in H2O2-producing cells and inducible nitric oxide synthase-expressing cells and the production of H2O2 and NO in both epidermis and dermis at a UV-B-irradiated site. Together, these data suggest that prevention of UV-B-induced infiltrating leukocytes, antigen-presenting cells, and oxidative stress by EGCG treatment of mouse skin may be associated with the prevention of UV-B-induced immunosuppression and photocarcinogenesis.

Animals↗

PubMedDate not supplied

[Perianal leukemic infiltration. Case report].

BACKGROUND: Leukemic infiltration of perianal skin (leukemia cutis) is quite uncommon, and may consist of no diffuse infiltration, erythema, ulceration, fistula, and abscess. Diagnosis may be established by biopsy and adequate hematologic studies. Treatment must be conservative in patients with poorly controlled disease (sitz baths, antibiotics, radiotherapy), and surgical in patients with risk of fulminant sepsis and death. OBJECTIVE: To report a case of leukemic perianal infiltration with atypical ulcerated lesion. CASE REPORT: Female patient, 21 years of age with diagnosis of AML M7, began with perianal pain posterior to evacuation associated with bleeding; at perianal examination we found anterior atypical ulcerated lesion. We carried out a biopsy under suspicion of leukemic infiltration corroborated by histopathology. The patient received conservative treatment. CONCLUSIONS: We must suspect leukemic infiltration in patients with anal symptoms and effect close surveillance. Prognosis depends on control of hematologic disease.

Adult↗

PubMed2003

Chronic lymphocytic leukemia with prostate infiltration mediated by specific clonal membrane-bound IgM.

Chronic lymphocytic leukemia (CLL) is characterized by an accumulation of monoclonal B lymphocytes in the hematopoietic organs. Rarely, CLL cells accumulate in a single atypical site. The mechanism underlying this unusual distribution of CLL cells has not been studied previously. We obtained peripheral blood from five patients having early stage CLL with heavy prostate infiltration. These patients' circulating CLL cells bound strongly in vitro to cultured prostate cell lines PC3, LNCaP, and DU145 and to short-term cultures of fresh prostate cells but not to colon, breast, or bladder cells. CLL cells from patients without prostate infiltration did not bind in vitro to any cell line. Peripheral blood CLL cells from one patient with CLL with heavy prostate infiltration were fused with a mouse-human heteromyeloma line to make hybridomas expressing the same monoclonal IgM as the patient's CLL cells. The hybridoma cells bound specifically to prostate cells. IgM secreted by the hybridoma blocked binding of the patient's CLL cells to prostate cells. Flow cytometry and immunohistochemistry demonstrated that the secreted IgM bound specifically to prostate cells. These results indicate that CLL with atypical prostate infiltration can be mediated by specific surface-bound IgM against an antigen expressed specifically by prostate cells and suggest that a similar mechanism might also apply to cases of CLL with atypical infiltration into other organs.

Animals↗

PubMed1992

Reaction patterns of tumor infiltrating lymphocytes in different renal cell carcinomas and oncocytomas.

1. Only clear cell and chromophilic carcinomas of the kidney exhibit a considerable lymphocytic infiltration which is compatible with some immunological responsiveness. Chromophobic carcinomas and benign oncocytomas seem to be immunologically reactive. This reflects the different antigen spectrum and histogenesis of these tumors (Störkel and Jacobi, 1989). Clear cell and chromophilic carcinomas are derived from the proximal tubule and chromophobic carcinomas and oncocytomas from the collecting duct. 2. The tumor periphery seems to be the place of greatest immunological importance, as basic requirements of a sufficient lymphocyte/tumor cell interaction can only be expected there. If these data are taken into account for a therapeutical approach with biological immune modifiers the size of the tumor (tumor burden) and proliferation index must be considered too. This might be a likely explanation for the positive effect of inhaled interleukin-2 on lung metastasis in renal cell cancers. Harvesting of tumor infiltrating lymphocytes for therapeutical purposes should take these findings into account. 3. In spite of dense lymphocytic infiltration only 3% of the tumor infiltrating lymphocytes exhibit the activation marker CD 25. There seems to be a sufficient T cell locomotion in renal cell carcinomas but an insufficient T-cell activation. Whether this fact is induced by lacking cytokine stimulation of involved lymphocytes or by still unknown mediators of the tumor cells is not yet known and needs further investigation. 4. Clear cell carcinomas exhibit most adhesion molecules and the highest amount of infiltrating cytotoxic T-cells and natural killer cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

PubMed1992

Tumor infiltrating cells in human cancer. On the possible role of CD16+ macrophages in antitumor cytotoxicity.

BACKGROUND: To obtain a better understanding of the mechanism underlying different modalities of immunotherapy, we investigated the types of tumor-infiltrating cells present at the tumor site, with special attention to the presence of macrophages. EXPERIMENTAL DESIGN: Frozen sections of carcinomas of the kidney, colon, breast, lung, ovary, and thyroid gland, as well as malignant melanoma were investigated with a panel of monoclonal antibodies against macrophage, T cell and NK cell associated antigens. Both type and pattern of the tumor-infiltrating cells were analyzed. RESULTS: All tumor-infiltrating cells accumulated preferentially in the stromal bands between tumor cells. In all types of tumor, CD11c+, CD14+, CD68+ and alpha-naphthyl-acetate-esterase positive monocytes/macrophages accounted for most tumor-infiltrating cells. Next in frequency were T lymphocytes (CD2+, CD3+, TCR alpha beta +). Only a few B lymphocytes (CD22+), and T cells expressing the T cell receptor gamma delta (TCR gamma delta) were found. Hardly any lymphoid cells with an NK phenotype (CD3-, CD56+) were present in the tumors studied. Large numbers of CD16+ cells were found, which could be identified as macrophages on the basis of their morphology, positive staining with a panel of monocyte/macrophage markers, and the results of double staining with CD11c. CONCLUSIONS: We have demonstrated the presence of a large number of macrophages in the cellular infiltrates of several types of tumors. The largest numbers of CD16+ macrophages were found in renal cancer, melanoma, and colonic-carcinoma. These are the tumors that are most susceptible to immunotherapy with lymphokine activated killer cells, suggesting that these CD16+ macrophages may be involved in antitumor cytotoxicity. Furthermore, these findings suggest that new strategies of immunotherapy aimed at the use of macrophages present in many tumors could be developed.

Antigens, CD↗