SEARCH · PubMed Health

Results for “classical monocytes”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources

PubMed1995

A lysosomal marker for activated microglial cells involved in Alzheimer classic senile plaques.

One of the major histopathological lesions in brains of patients with dementia of the Alzheimer type (DAT) is the senile plaque. Although previous studies have shown that senile plaques are often accompanied by microglial cells, the role of these cells in DAT pathology is still unclear. In an immunohistochemical and immunoelectron microscopical analysis of DAT and control brain tissues we addressed this issue using two monoclonal antibodies (mAbs KP1 and 25F9) directed against lysosomal antigens in monocytes and macrophages. Whereas KP1 stained lysosomes in both resting and activated microglial cells, 25F9-staining was predominantly found in lysosomes of activated microglial cells in classic senile plaques. The number and size of 25F9-positive lysosomes in activated microglial cells was increased compared to 25F9-staining in unaffected areas in DAT and control sections. We conclude that mAb 25F9 is a unique and useful lysosomal marker, with a higher specificity than other known markers, for activated microglial cells associated with classic, but not with diffuse, senile plaques.

Aged↗

PubMed1993

Morpho-immunophenotypic diversity of Castleman's disease, hyaline-vascular type: with emphasis on a stroma-rich variant and a new pathogenetic hypothesis.

A histologic review of 102 cases of Castleman's disease of the hyaline-vascular type, with a detailed paraffin immunophenotypic study of 23 of them, was undertaken to evaluate the morphologic variability of this disorder and its immuno/cyto-architectural characteristics. All cases had features in common including: abnormal follicles, with increased vascularity, poorly formed germinal centers and predominance of the mantle zone; lack of sinuses; and hypervascular interfollicular tissue containing large numbers of KP1-positive plasmacytoid monocytes. Networks of actin-positive cells [fibroblastic reticulum cells (RCs) or "myoid cells"] and KP1-positive dendritic cells (histiocytic RCs) were seen. There were differences in the proportion of follicles to interfollicular tissue, which covered a continuum from a "follicular", through a "classic", to a "stroma-rich" variant. The last-mentioned was qualitatively different as it showed loss of HECA-452 and MECA-79 reactivity in the blood vessels, decreased plasmacytoid monocytes and increased myoid cells and histiocytic RCs. In 5 cases there was formation of distinct nodular growths which varied from spindle cell foci to angio-histiocytic-RC proliferations, all of which may be confused with vascular or follicular dendritic RC neoplasms. From our findings, data from the literature and the working hypothesis that plasmacytoid monocytes are the precursors of both follicular dendritic RCs and sinus lining cells (Parwaresch et al.), a pathogenetic theory is proposed for this type of Castleman's disease which postulates that a developmental block in plasmacytoid monocytes results in their accumulation with poor formation of germinal centers and sinuses under stimulation. The lack of sinuses would lead to impaired egress of circulating lymphocytes which, however, would continue to enter the node through functional high endothelial venules and to accumulate in the mantle zone. The factors responsible for angiogenesis and for the cellular growths that characterize the stroma-rich variant remain to be determined, as do the relationships between the three variants.

Adolescent↗

PubMed1991

Transforming growth factor beta 1, a potent chemoattractant for human neutrophils, bypasses classic signal-transduction pathways.

Transforming growth factor beta 1 (TGF-beta 1), a homodimeric polypeptide (Mr 25,000), derives from inflammatory cells and acts as a chemoattractant for monocytes and fibroblasts. We report here that TGF-beta 1 is also the most potent chemoattractant yet described for human peripheral blood neutrophils. Recombinant TGF-beta 1 elicited dose-dependent directed migration of neutrophils under agarose that was inhibited in the presence of a neutralizing antibody to TGF-beta 1. Maximal chemotaxis was evoked by TGF-beta 1 at femtomolar concentrations, whereas conventional chemoattractants act at nanomolar concentrations: on a molar basis, TGF-beta 1 was 150,000 times more potent than fMet-Leu-Phe. In contrast, TGF-beta 1 provoked neither exocytosis nor the production of superoxide by neutrophils. We further analyzed the mechanism by which TGF-beta 1 elicits chemotaxis (GTPase activity, [Ca2+], and actin polymerization). In contrast to the conventional chemoattractant fMet-Leu-Phe, TGF-beta neither activated classic heterotrimeric guanine nucleotide-binding proteins nor provoked global mobilization of intracellular Ca2+. Chemoattraction by both fMet-Leu-Phe and TGF-beta 1 was inhibited by cycloheximide and actinomycin D. Moreover, chemotaxis in response to TGF-beta 1 was associated with the polymerization of actin. The selectivity and potency of TGF-beta 1 as a chemoattractant suggest that it elicits directed cell migration by means of a pathway that depends not on classic intracellular signals but on protein synthesis.

Calcium↗

PubMed1996

Inhibition of monocyte chemotaxis to C-C chemokines by antisense oligonucleotide for cytosolic phospholipase A2.

Monocyte chemotactic protein (MCP)-1, a member of the C-C (or beta) branch of the chemokine superfamily, at chemotactic concentrations, induced a rapid release of [3H]arachidonic acid but not of [14C]oleic acid from prelabeled human monocytes. This effect was associated with an increase in the intensity of the immunoreactive band corresponding to the phosphorylated form of cytosolic phospholipase A2, (cPLA2). To address the role of cPLA2 in the induction of monocyte chemotaxis, cells were treated with a specific antisense oligonucleotide. Monocytes cultured in the presence of 10 microM antisense oligonucleotide for 48 h showed a marked decrease (57 +/- 5%; n = 4) of cPLA2 expression, as evaluated by Western blot analysis and a nearly complete inhibition (81.8 +/- 4.2%; n = 3) of [3H]arachidonic acid release in MCP-1-stimulated cells. Monocyte chemotaxis in response to MCP-l also was inhibited in a concentration-dependent manner by cPLA2 antisense oligonucleotide (IC50 = 1.9 +/- 1.1 microM; n = 3), with complete inhibition observed between 3 and 10 microM. No inhibition of chemotactic response was observed in monocytes treated with a control oligonucleotide. Monocyte migration in response to MCP-3, RANTES (regulated on activation normal T cells expressed and secreted), and MIP-1 alpha/LD78 also was inhibited (>70%) in antisense oligonucleotide-treated cells. On the contrary, the chemotactic response elicited by formyl-methionyl-leucyl-phenylalanine and C5a, two "classical" chemotactic agonists, was minimally affected (<20%) by antisense oligonucleotide treatment. These data show that cPLA2 plays a major role in [3H]arachidonic acid release by MCP-1 in human monocytes and provide direct evidence for the involvement of cPLA2 in C-C chemokine-induced monocyte chemotaxis.

Arachidonic Acid↗

PubMed2006

The anti-microbial peptide LL-37 inhibits the activation of dendritic cells by TLR ligands.

The endogenous anti-microbial peptide LL-37/hCAP-18 is an effector molecule of the innate host defense system at surfaces of the body. Besides its direct anti-microbial activity, the peptide interacts with different cell types. Dendritic cells (DCs) play a central role in mucosal host defense. It was the aim of the study to determine whether LL-37 modulates the response of DCs to pathogen-associated molecular patterns. Monocyte-derived DCs were stimulated with the Toll-like receptors (TLRs) ligands LPS, lipoteichoic acid and flagellin. We measured classical markers of DC maturation and assayed the ability of the DCs to activate T cell responses. Co-incubation with LL-37 resulted in suppressed activation of DCs. Levels of released IL-6, IL-12p70 and TNF-alpha and surface expression of HLA-DR, CD80, CD83, CD86 and the chemokine receptor CCR7 were decreased. Exposure of DCs to LL-37 during LPS exposure induced co-cultured naive T cells to produce less IL-2 and IFN-gamma and decreased their proliferation. The response of memory T cells to a recall antigen was also decreased. In conclusion, we demonstrate that the anti-microbial peptide LL-37 inhibits the activation of DCs by TLR ligands. We propose that LL-37 is a regulator of host defense responses at the intersection of innate and adaptive immune systems.

Amino Acid Sequence↗

PubMed1983

Human natural killer cells, activated lymphocyte killer cells, and monocytes possess similar cytotoxic mechanisms.

The relationship between the killing mechanisms of human natural killer (NK) cells, mitogen- and mixed-lymphocyte-culture-induced activated lymphocyte killer (ALK) cells, and monocytes was investigated with a monoclonal antibody. The IgG2 antibody 9.1C3 was prepared from mice immunized with purified human large granular lymphocytes and selected from clones that inhibited NK cell killing. The 9.1C3 antibody bound to all mononuclear cells but not to granulocytes or K562 cells, and it selectively blocked killing of K562 targets by both NK and ALK cells without affecting the binding of effector to target cells. The antibody blocked killing when present from time zero and it still inhibited partially even when added 1 hr after initiation of the lytic reaction. Killing of Epstein-Barr virus-transformed B lymphoblasts by classical cytotoxic T lymphocytes was not inhibited. Of interest, 9.1C3 did block the killing of K562 target cells by cultured peripheral blood monocytes. Other monoclonal antibodies that bound to monocytes did not block killing, and a nonspecific effect of the antibody on monocytes was excluded. These data suggest that NK cells, ALK cells, and monocytes can kill tumor cell targets by using similar lytic mechanisms.

Animals↗

PubMedDate not supplied

[How does the immune system communicate with the brain?].

It is now evident, that the immune system and the central nervous system (CNS) are functionally connected and interact with one another. The entrance of pathogenic micro-organisms or their products into the body evokes an array of systemic responses, i.e. acute-phase proteinemia, neutrophilic leucocytosis, changes in the circulating levels of various hormones, and fever with specific changes of behaviour. It is now generally recognised that many of these responses are modulated by the brain. Until 1995 it was thought that the transport of immune signals to the brain is mediated by a humoral mechanism, mainly by certain cytokines, produced by activated monocytes and macrophages. The mechanism for the transfer of cytokines through the blood-brain barrier was however not completely understood until recently. It was also not clear, how the fast febrile phase can be signalled within 15 min, if the sequence: external pyrogen-->monocytes-->cytokines-->prostaglandins-->stimulation of the hypothalamus-->fever, requires 40-60 minutes to be activated. In addition to the "classical" humoral mode of transfer, it has recently been proposed that the immune signals are transported to the brain by certain peripheral nerves, predominantly by the vagus. The macrophages of the liver (Kupfer cells) start producing small amounts of cytokines in response to their activation by bacterial lipopolisaccharides, coupled into a complex with the already pre-activated anaphylatoxic component of the complement. These cytokines can immediately activate adjacent sensory paraganglia of the hepatic vagus nerve, which carries these stimuli to the nucleus tractus solitarius, which in turn sends them out to the hypothalamus via the ascending noradrenergic pathways. This fast avenue of communication between the immune system and the brain is activated not only in pathological situations, corresponding to fever, but is an important component of systemic homeostasis, e.g. regulation of body temperature.

Brain↗

PubMedDate not supplied

[IgM monoclonal gammopathy in plasmacytic neoplasms].

In 331 patients with the diagnosis of multiple myeloma in 4 cases proliferation of plasma cells was associated with synthesis of a monoclonal IgM. In 3 of these cases coexistence was noted of features typical of multiple myeloma and Waldenström's macroglobulinaemia. In the clinical picture in two of these cases sings of blood hyperviscosity prevailed. These patients showed impairment of plasma clotting factors. The count of T and B cells in blood and the adherence and phagocytic activity of monocytes were not abnormal. The ultrastructural pattern of plasma cells in bone marrow was similar to that observed in classical cases of IgG or IgA multiple myeloma. In one case of lymphoplasmocytic proliferation with leucocytosis over 100 x 10(9)/l immunoelectroscopic examination of bone marrow cells demonstrated a formidable accumulation of the heavy chain of mu immunoglobulin in the cytoplasm of lymphoplasmacytes. In the serum and urine no monoclonal protein was found. In this case compression of vertebral bodies Th7 and L2 occurred.

Adult↗

PubMed1994

P190BCR-ABL chronic myeloid leukaemia: the missing link with chronic myelomonocytic leukaemia?

Two-thirds of patients with Philadelphia (Ph) chromosome-positive acute lymphoblastic leukaemia (ALL) have a breakpoint in the minor breakpoint cluster region (m-bcr) of the BCR gene, which results in an e1a2 transcript and a P190BCR-ABL fusion protein. This type of genomic rearrangement occurs very rarely in chronic myeloid leukaemia (CML); it has been reported in only four cases. We describe here a fifth case of P190 CML in which the cytomorphological characteristics were intermediate between CML and chronic myelomonocytic leukaemia (CMML). This case, and the four reported previously, had a consistent and significant monocytosis with a low neutrophil/monocyte ratio in the peripheral blood, resembling CMML. On the other hand, they also had a high percentage of circulating immature granulocytes, basophilia and low neutrophil alkaline phosphatase (NAP) score, which are more commonly found in classical CML. Thus, P190 CML may be a specific form of CML, in which the myeloproliferative process includes the monocytic, as well as the granulocytic lineage. Since the molecular defect in CML is thought to involve a pluripotent stem cell, the different effects of P210BCR-ABL and P190BCR-ABL in CML must reflect the somewhat wider spectrum of activity of the P190BCR-ABL. Other patients with atypical CML or CMML who lack a Ph chromosome may also have an m-bcr breakpoint which would not be detected on standard Southern blots, but which would be detectable by polymerase chain reaction amplification of reverse transcribed RNA.

Adult↗

PubMed1987

Establishment of three permanent human leukaemia cell lines producing immunoreactive calcitonin.

Three permanent human leukaemia cell lines, designated EW2, LG3 and MS6, were established from bone marrow aspirates of a patient with acute myelomonocytic leukaemia (EW2), acute monocytic leukaemia (LG3) and acute myeloblastic leukaemia (MS 6). In vitro all lines exhibited a myelomonocytoid marker profile in terms of classical staining reactions and cell-surface antigen structure. In supernatants and extracts of EW2 and MS 6 cells immunoreactive human calcitonin was found in raised levels. No significant levels of immunoreactive human calcitonin were found in supernatants of LG3 cells, while extracts of LG3 cells and the patients sera at diagnosis contained high levels, suggesting the in vitro selection of a non-secreting clone of leukaemic cells. Gel-chromatography showed several peaks of ihCT with higher molecular weight than normal human calcitonin, suggesting the production of precursor molecules. In addition to ihCT raised levels of immunoreactive calcitonin gene related peptide (ICGRP) was found in supernatants of EW2. These data support the concept of ectopic immunoreactive human calcitonin production by leukaemic cells.

Antigens, Neoplasm↗

PubMed1992

Effect of morphine on phagocytic activity of the polymorphonuclears and monocytes.

The effect of morphine on the phagocytic activity of the polymorphonuclears (PMN), and monocytes in peripheral blood of laboratory rats of inbred Wistar strain was studied in vitro. Phagocytic activity of both types of the white blood cells was examined by the classical method using microspherical hydrophilic particles (Hema-particles), phagocytosis of the Hema-particles was determined by light microscopy. For evaluation of the leukocyte adherence, the method of MacGregor was used. Morphine was proved to influence phagocytic activity of individual types of the leukocytes in different way. Phagocytic activity of the PMNs was suppressed (by 14.0%), and that of monocytes was potentiated (by 17.1%).

Animals↗

PubMed2003

Caspase 1 involvement in human monocyte lysis induced by Actinobacillus actinomycetemcomitans leukotoxin.

Actinobacillus actinomycetemcomitans, an oral bacterium implicated in the etiology of periodontal diseases, produces a leukotoxin that selectively lyses primate neutrophils and monocytes, the major populations of defense cells in the periodontium. Though lysis requires expression of the receptor lymphocyte function-associated molecule 1 (LFA-1) on the cell surface, not all LFA-1-expressing leukocyte populations are equally susceptible to the toxin. In this study, the susceptibility of human leukocytes to leukotoxin-induced lysis is compared to their expression of LFA-1 and the activity of caspase 1. Cytolysis was determined by the activity of lactate dehydrogenase released from peripheral human leukocytes after 1-h exposure to leukotoxin. Monocytes were lysed at leukotoxin concentrations of > or = 5 ng/ml, while the corresponding values for neutrophils and lymphocytes were approximately 10 times greater. Similar LFA-1 expression was found in all susceptible cell populations irrespective of their degree of sensitivity to the toxin. Exposure of monocytes to leukotoxin increased their caspase 1 activity about fivefold within 10 to 20 min. Presence of the caspase 1 inhibitor Ac-YVAD-CMK significantly blocked the leukotoxin-induced lysis of monocytes only. At sublytic concentrations, leukotoxin induced no apoptotic activity in monocytes, as revealed by the lack of caspase 3 activation and DNA fragmentation. Monocytes are the most lysis-sensitive leukocytes for A. actinomycetemcomitans leukotoxin. Their lysis by this toxin depends on caspase 1 activation and proceeds through a process that differs from classical apoptosis.

Actinobacillus Infections↗

PubMed1986

Immunological studies in patients with alcoholic liver disease: evidence for the in vivo activation of helper T cells and of the monocyte-macrophage system.

Immunologic parameters were evaluated in 22 patients with alcoholic liver disease (ALD). Patients with ALD had increased levels of circulating immune complexes (CIC) and serum immunoglobulins, particularly IgA. The classical complement pathway was preferentially activated in CIC-positive patients. There was no increase in total lymphocyte or total T lymphocyte counts, but a significant rise in both the helper/inducer population (OKT4) and helper/suppressor cell ratio (T4/T8) was noted. The presence of interleukin-2 receptors and HLA-DC/DS and HLA-DR antigens suggested in vivo activation of ALD patients' T cells. The rate of differentiation of B cells to plasma cells was high in both pokeweed mitogen-stimulated and unstimulated cultures of ALD patients' B cells, whereas plasma cell generation doubled when patient T lymphocytes were added to enriched normal B cells. The above data support a role for activated helper (T4+) T cells in the immune response initiated by alcoholic hepatitis. Serum angiotensin-converting enzyme levels and lysozyme levels were increased in ALD patients, and cultured adherent mononuclear cells from ALD patients secreted more lysozyme in vitro than normal cells, suggesting the presence of an activated monocyte-macrophage system in ALD.

Adult↗

PubMed2001

Induction of apoptosis in bone marrow neutrophil-lineage cells by classical swine fever virus.

The pathogenesis of bone marrow atrophy during classical swine fever (CSF) was investigated in vitro by using CSF virus (CSFV) infection of bone marrow haematopoietic cells (BMHC). The monocytic lineage had the highest susceptibility to CSFV infection, whereas the more mature SWC8(+) granulocytic cells were not directly susceptible to infection. However, myelomonocytic precursors were targets for CSFV infection and continued to differentiate into SWC8(+) granulocytic cells, which remained infected. This explains the occurrence of infected peripheral blood granulocytes during CSF. The infection of BMHC resulted in increased apoptosis and necrosis, mainly within the granulocytic lineage. Caspases 3 and 9 were particularly activated, relating to the mitochondrial pathway of apoptosis. Interestingly, the majority of infected cells were non-apoptotic, the apoptotic cells being primarily non-infected. This indicated an indirect mechanism for induction of apoptosis, but no role could be identified for bone marrow stroma cells such as macrophages or fibroblastoid cells. Furthermore, soluble factors including cytokines and reactive oxygen species were not primarily responsible. In contrast, contact between infected and non-infected BMHC was critical for increasing apoptosis in the latter. Taken together, these results in vitro relate to and help to explain further the apoptosis of BMHC that occurs in vivo during CSF. This experimental system will also be particularly useful for the study of CSFV gene products involved in leukocyte apoptosis.

Animals↗

PubMed2003

Initial RNA expression in human monocytes after multiple injury: a screening pilot study on potentially trauma-sensitive factors by using the microarray-technique.

BACKGROUND: Pathological affection of the immune system is one of the initiating mechanisms for the induction of multiple organ failure (MOF) in patients suffering from multiple injuries. Potential responsible intracellular mechanisms such as initial monocyte mRNA expression of specific mediators remain poorly studied, so far. Hence, we applied the microarray technique for screening of a wide variety of genes in circulating monocytes of multiple injured patients and compare the molecular results to the clinical course of the patients (MOF-score). METHODS: In our prospective pilot study 6 patients were enclosed presenting with blunt multiple injuries (Injury Severity Score 16 to 57 points). Monocytes were isolated out of sequentially drawn samples (6, 12, 24 and 48 hours after trauma) using magnetic cell sorting (CD14) and a human microarray system was used (Atlas stress 1.2, Clontech, 1176 genes). Alterations in the sequential samples were identified by calculating ratios to baseline levels on admission and cluster analysis was performed (Spotfire Decision). RESULTS: Only 86 (ca.5%) genes displayed an obvious signal. The house-keeping genes clustered well together in all patients in contrast to a substantial inter-individual variability of the other signal giving genes. No mediator burst of the classical pro- or anti-inflammatory cascade were detected. CONCLUSION: We demonstrate for the first time a screening analysis of mRNA expression patterns in circulating monocytes of multiple injured patients indicating that only very few genes appeared to be influenced by the traumatic event. So far, no correlation to the severity of trauma or MOF could be detected.

Adult↗

PubMed2004

IgSF13, a novel human inhibitory receptor of the immunoglobulin superfamily, is preferentially expressed in dendritic cells and monocytes.

A novel inhibitory receptor of immunoglobin superfamily (IgSF), IgSF member 13 (IgSF13), has been identified from human dendritic cells (DC). IgSF13 is a type I transmembrane protein containing an N-terminal signal peptide, a extracellular region with a single Ig V-like domain, a transmembrane region, and a cytoplasmic tail with two classical immunoreceptor tyrosine-based inhibitory motifs (ITIM), suggesting its inhibitory function. IgSF13 shows significant homology to human CMRF35 and pIgR. IgSF13 gene is mapped to chromosome 17q25.2, very close to that of CMRF35. IgSF13 is preferentially expressed in myelo-monocytic cells, including monocytes, monocyte-derived DC, and monocyte-related cell lines. Upon pervanadate treatment, IgSF13 was hyper-phosphorylated and associated with Src homology-2 domain-containing phosphatases SHP-1 and SHIP, but not SHP-2. The identification of IgSF13 as a novel ITIM-bearing receptor selectively expressed by DC and monocytes suggests that it may be potentially involved in the negative regulation of specific leukocyte population.

Amino Acid Sequence↗

PubMed2003

A neuroendocrine-immune interface. The immunostimulatory state of aldosteronism.

Hypertension is an important determinant of heart failure. Ventricular systolic and/or diastolic dysfunction can eventuate in an activation of the renin-angiotensin-aldosterone system (RAAS). Circulating RAAS effector hormones lead to: the appearance of the congestive heart failure syndrome; and a systemic illness that features oxi/nitrosative stress in various tissues, including blood, together with circulating pro-inflammatory cytokines, anorexia and, ultimately, cachexia. In addition to its well-known endocrine properties, expressed in epithelial cells of classic target tissues, aldosterone (ALDO) has an emerging portfolio of actions in nonclassic target tissues, such as circulating lymphocytes and monocytes (or peripheral blood mononuclear cells [PBMC]). This neuroendocrine-immune interface is based on Na(+)-dependent, ALDO-induced iterations in PBMC cytosolic free [Mg(2+)](i) and [Ca(2+)](i). Ca(2+) loading contributes to an induction of oxi/nitrosative stress and activation of PBMC transcriptome. This immunostimulatory state begets a pro-inflammatory/fibrogenic vascular phenotype involving the heart and systemic organs and can be prevented by either ALDO receptor antagonism or antioxidant. The established efficacy of ALDO receptor antagonism as an integral component of the overall management of symptomatic heart failure may include its immunomodulatory properties. This brief review traces studies that led to and then identified the neuroendocrine-immune interface that accompanies aldosteronism.

Aldosterone↗

PubMedDate not supplied

Characterisation of immunoglobulin-binding leucocytes in carp (Cyprinus carpio L.).

This study demonstrates the immunoglobulin(Ig)-binding capacity of Ig-positive carp macrophages employing immunofluorescence and immunogold methods. These methods allow for the characterisation of the Ig-binding cells. After internalisation of fluorescent- or gold-labelled Ig (30 min at room temperature), most macrophages from the hindgut were able to bind added purified carp Ig, which could be demonstrated clearly with a second fluorescent or gold label. In pronephros, an important haemopoietic organ in fish, a limited number of monocyte-like cells also showed Ig binding. Pronephros macrophages and neutrophilic granulocytes appeared to be Ig-negative. The use of goat anti-mouse Ig gold particles bound by carp anti-goat antibodies revealed that, in addition to hindgut macrophages and pronephric monocyte-like cells, some lymphoid cells in both hindgut and pronephros cell suspensions were also able to bind Ig. The classic erythrocyte-antibody rosette assay resulted in a limited number of small rosettes in cell suspensions from both organs.

Animals↗