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PubMed2000

All trans retinoic acid induces apoptosis in acute promyelocytic NB4 cells when combined with isoquinolinediol, a poly(ADP-ribose) polymerase inhibitor.

NB4 cells, a model of acute promyelocytic leukemia have been shown to undergo granulocytic differentiation in response to all trans retinoic acid (ATRA), or monocytic differentiation in response to 1alpha,25 dihydroxyvitamin D(3) (1,25 D(3)) and phorbol ester. We have shown previously that the expression of poly(ADP-ribose) polymerase (PARP) is dramatically increased during monocytic differentiation and completely down-regulated during neutrophilic differentiation. Here we show that NB4 cells simultaneously treated with ATRA and isoquinolinediol (Iso-Q), a specific PARP inhibitor, fail to differentiate into neutrophils. Nitroblue tetrazolium (NBT) dye reduction was inhibited by 48% and neutrophil formation was reduced by 75%. NB4 cells treated with ATRA and Iso-Q instead showed features of apoptosis including nuclear condensation, DNA fragmentation, and PARP cleavage yielding a 85 kDa fragment. NB4 cells treated with ATRA in combination with 1,25 D(3), a monocytic differentiation inducer, while continuing to reduce NBT also failed to mature into neutrophils or monocytes and again showed features of apoptosis. Down-regulation of Bcl-2 protein expression was evident in NB4 cells treated with ATRA and ATRA in combination with Iso-Q or 1,25 D(3), but not in cells treated with a classic chemotherapeutic agent, arabinosycytosine, suggesting that Bcl-2 down-regulation is neither necessary, nor specific for apoptosis in this model.

Apoptosis↗

PubMed2004

Mechanisms of leukocyte recruitment to atherosclerotic lesions: future prospects.

PURPOSE OF REVIEW: Leukocyte invasion in the arterial wall is critical in the development of atherosclerotic lesions. This review describes recent advances in the understanding of leukocyte recruitment in atherogenesis and in the development of vulnerable plaque. It also discusses limitations in the current knowledge of this process and how these limitations may be addressed. RECENT FINDINGS: The adhesive function of platelets has recently been highlighted as an important recruitment mechanism in atherosclerosis. For example, targeted deficiency of P-selectin in platelets reduces atherosclerosis in mice. Platelets also increase monocyte recruitment in atherosclerosis by secreting chemokines such as platelet factor 4 (CXCL4) or RANTES (CCL5), which trigger monocyte arrest in atherosclerotic arteries. A causal role for RANTES in atherosclerosis was shown by a protective effect of the blockage of RANTES receptors in apolipoprotein E-deficient mice. A similar effect was also demonstrated for the fractalkine receptor CX3CR1. Moreover, the classic chemoattractant LTB4 plays important roles in atherosclerosis, inasmuch as the absence of the principal LTB4 receptor (BLT1) reduces early atherosclerosis in mice. Novel data have also shown that many types of cells in lesions express 5-lipoxygenase, which indicates a rich source of leukotrienes in plaque. SUMMARY: Recent data provide evidence for the involvement of several adhesive and signalling mechanisms in leukocyte recruitment in atherosclerosis. However, the specific mechanisms that are responsible for the accumulation of proatherogenic leukocytes in lesions are unclear. Detailed study of certain subclasses of leukocytes in the recruitment process will be important in future studies in this field.

Animals↗

PubMed1975

Congenital neutropenia: impaired maturation with diminished stem-cell input.

Children with congenital neutropenia (Kostman disease) present a syndrome of recurrent and eventually fatal bacterial infections. The disease is uniformly lethal and the mean age at death is 24 months. To attempt to better understand the nature of this inborn error, we have studied marrow and peripheral blood of 3 children with the disease. Along with classic morphologic analysis we have used the technic of soft agar bone marrow culture in vitro. All 3 patients showed marked deficiency of numbers of neutrophils in the peripheral blood, intermittent monocytosis especially with infection, and predominant nitroblue tetrazolium (NBT) dye staining in monocytes during infection. The marrow of all 3 patients showed evidence of maturation arrest at the promyelocyte stage and very few or no neutrophils. Two cases showed no neutrophils in the Rebuck skin window inflammatory study. The 3rd case, however, developed small numbers of neutrophils in the peripheral blood, up to 6%, but the first 2 patients, although studied on many occasions, did not show neutrophils above 1%. Evidence from soft agar culture of bone marrow in 1 patient was compatible with the view that development of committed neutrophil stem cells is defective. This patient did not develop neutrophils in soft agar culture and showed loose colonies developing only to promyelocytes. In the 2nd case, where depression of neutrophil development was somewhat less severe clinically, culture of the marrow in soft agar yielded normal neutrophil colonies and none of the loose colonies showing arrested maturation were seen. These findings suggest that the basic mechanism underlying the congenital neutropenias may differ from patient to patient.

Agranulocytosis↗

PubMed2000

Inhibition of endothelial cell activation by nitric oxide donors.

Because nitric oxide (NO) inhibits the expression of endothelial leukocyte adhesion molecules, NO-generating compounds have major therapeutic potential for use outside their classical indications. We report on the in vitro potential antiatherogenicity of two novel cysteine-containing NO donors, SP/W 3672, a fast spontaneous NO releaser, and its prodrug SP/W 5186, which liberates NO after bioactivation. The ability of these two compounds to inhibit monocyte adhesion and surface expression of endothelial adhesion molecules was evaluated and compared with that of other NO donors. SP/W 5186 and SP/W 3672 inhibited the adhesion of U937 monocytes to cultured human endothelial cells more potently than S-nitrosoglutathione (GSNO) or spermine NONOate, whereas nitroglycerin and isosorbide dinitrate were ineffective at comparable concentrations. A similar rank order of potency was found for the inhibition of expression of the adhesion molecules vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and E-selectin as well as for major histocompatibility complex class II antigen expression. Estimated IC(50) values for vascular cell adhesion molecule-1 were >400 microM for SP/W 4744 (control for SP/W 3672 lacking the cysteine moiety), 200 microM for GSNO and spermine NONOate, 80 microM for SP/W 3672, and 50 microM for SP/W 5186. Moreover, SP/W 5186 inhibited VCAM-1 mRNA levels more potently than GSNO. This effect was likely to be transcriptional because mRNA degradation was not affected. In conclusion, SP/W 3672 and SP/W 5186 are novel potent inhibitors of endothelial activation, and this effect appears to relate to their ability to liberate NO for prolonged periods of time, either spontaneously or after conversion to active hydrolytic products.

Cell Adhesion↗

PubMed1993

[The cellular and molecular-biological studies on Philadelphia chromosome-positive acute lymphocytic leukemia].

Philadelphia chromosome (Ph1) is detected in more than 95% of chronic myelogenous leukemia (CML) and approximately 20% of adult acute lymphocytic leukemia (ALL). In order to discriminate Ph1-positive ALL from Ph1-positive CML as a clinical entity, I studied on biological and genetic characteristics of Ph1-positive ALL cells. Two cases out of 11 Ph1-positive ALL showed hybrid leukemia phenotypes; in one hybrid case simultaneous proliferation of lymphoid and myeloid blast cells was observed and contained rearranged alleles of heavy chain genes, thus indicating that both blast cells might originate from a common precursor. Two Ph1-positive ALL cell lines (TOM-1 and ALL-MIK) were established from two patients and were investigated for their differentiation potential in vitro. Both cell lines showed the potency to differentiate into monocytic lineage cells, thus suggesting that these Ph1-positive ALL cells might reside at the stage of multipotent progenitor cell along hematopoietic cell differentiation. As to Ph1-chromosome, 4 out of 9 Ph1-positive ALL cases showed rearrangements within the classical sequence (M-bcr), similar to those in CML cases. Two out of 5 cases without rearrangement of M-bcr showed breakpoints in the first intron of the BCR gene. In the rest of 3 cases, BCR-ABL rearrangement was not detected by Southern analysis. However, a leukemic cell line established from one of these patients (TOM-1) were contained P190bcr-abl mRNA as analyzed through RT-PCR. Thus, breakpoints of the BCR gene in Ph1-positive ALL cases were heterogenous, in contrast to those of CML. Then, I investigated whether or not the activation of transforming genes other than BCR-ABL might be involved in pathogenesis of Ph1-positive ALL. Three out of 15 Ph1-negative ALL cases showed the mutations of RAS gene by the PCR. However, no activated oncogene was detected in Ph1-positive ALL cases by both DNA transfection assay and PCR.

Adult↗

PubMed1998

Properties of mu 3 opiate alkaloid receptors in macrophages, astrocytes, and HL-60 human promyelocytic leukemia cells.

An opiate alkaloid-selective receptor, designated mu(3), mediates inhibition by morphine of activation of human peripheral blood monocytes and granulocytes. The mu(3) receptor is present on several macrophage cell types including microglia, on cultured astrocytes, and in brain and retina. Murine macrophage cell lines and human HL-60 leukemia cells contain high concentrations of these receptors. Binding of 3H-morphine to the receptor is displaced by morphine, etorphine, naloxone, diprenorphine and morphine 6-glucuronide, but not by morphine 3-glucuronide, fentanyl, benzomorphans, enkephalins, dynorphin, beta-endorphin, endomorphin-1, other opioid peptides or nociceptin (orphanin FQ). The mu(3) receptor appears to be much more sensitive to inactivation by reduced glutathione than are classical mu, delta and kappa receptors. Evidence is also presented for G protein-coupling of these receptors. These and other data raise the possibility that the mu(3) receptor is a member of a chemokine or of another related receptor family, rather than the opioid receptor family. The affinity for morphine of mu(3) receptors of granulocytic-differentiated HL-60 cells is markedly enhanced in the presence of levorphanol and certain benzomorphans. In contrast, receptors of monocytes, macrophage cell lines, microglia, macrophage-differentiated HL-60 cells and astrocytes are not affected by levorphanol or benzomorphans. It is concluded that mu(3) receptors of granulocytic and promyelocytic cells differ from those of macrophage and astrocyte cell types, possibly due to differences in receptor subtype or to the presence of an additional component in the granulocytic and promyelocytic cells.

Animals↗

PubMed1998

[Is arteriosclerosis an infectious disease?].

There are three findings suggesting the inflammatory and immunogenic nature of the atherosclerosis: Firstly the colocalisation of macrophages/monocytes and T-lymphocytes in all phases of the atherosclerosis, starting with intimal damages and developing into the end stage of atheromatous plaques, secondly the production of cytokines and thirdly the expression of MHC II antigens. The persisting chlamydia pneumoniae bacteria infection, which has been repeatedly detected in the intima, sustains this inflammatory process. Endothelial dysfunction and an expression of adhesion molecules, which might have been triggered by the chlamydial infection, could lead to atherosclerotic lesions according to the "response to injury" theory. The chlamydiae specific findings can well be integrated into this concept: Two of three classical Koch postulates are nearly fulfilled. There is additional direct and indirect evidence--particularly the first positive results of oral antibiotic therapy after acute myocardial infarction--suggesting a causative role. The unfavourable changes in the lipid profile, which might be brought about by the infection, may also contribute. Repeated chlamydial reinfections trigger the immune system through the cellular memory of T-lymphocytes sustaining the intramural inflammatory process. This leads to an activation of metalloproteinases with a fissuring on the plaques and finally to thrombosis. If this suggested link is confirmed, the latent chlamydia infections could be another treatable risk factor apart from the classical cardiovascular risk factors.

Acute-Phase Reaction↗

PubMed1995

[Experimental therapy of hypoplastic paroxysmal nocturnal hemoglobinuria].

Paroxysmal nocturnal hemoglobinuria (PNH) and aplastic anemia are associated either as a PNH-aplasia syndrome or the emergence of glycosylphosphatidylinositol-(GPI)deficient blood cells in patients with severe aplastic anemia (SAA). It could be demonstrated that SAA patients with GPI-deficient cells in comparison to those without have a worse response to classical immunosuppressive therapy. Therefore, we treated a female PNH patient with severe thrombocytopenia, anemia and granulopenia with G-CSF and cyclosporine. Within 8 weeks, a trilineage response of hematopoiesis was observed. In addition, the proportion of normal to GPI-deficient granulocytes and monocytes increased significantly.

Adult↗

PubMed1993

Functional aspects of the C1q receptors.

C1q, the recognition subunit of the classical complement pathway, has been shown to stimulate host defense mechanisms. It has become increasingly evident that C1q can bind to several different cell types resulting in a variety of functional consequences depending on the cell type. For example, the binding of C1q to monocytes enhances the ability of those cells to ingest pathogens, while interaction with neutrophils, eosinophils, endothelial cells and vascular smooth muscle cells triggers or enhances the generation of toxic oxygen species. While these latter oxygen products play a major role in the destruction of foreign pathogens, in some cases, such as immune-complex-induced vasculitis and myocardial infarction, these toxic oxygen molecules can cause excessive host tissue damage. The differential modulation of C1q-mediated activities by monoclonal antibodies suggest that there is more than one unique type of C1q receptor, which is not necessarily surprising given the diversity of responses reported. This review summarizes what is known about the functional consequences of the interaction of C1q with cells, and describes initial investigations of the biochemical mechanisms/signal transduction pathways involved in these C1q-induced responses. Further investigations of the C1q/C1q receptor system(s) should uncover basic mechanisms and modes of regulation of these defensive responses by the host, and potentially provide information useful for beneficial manipulation of these activities.

Animals↗

PubMed2000

Inhibition of L-leucine methyl ester mediated killing of THP-1, a human monocytic cell line, by a new anti-inflammatory drug, T614.

T614 (3-formylamino-7-methylsulfonylamino-6-phenoxy-4H-1-benzopyran-4-o ne) is a member of the family of methanesulfonanilide non-steroidal anti-inflammatory drugs (mNSAIDs), most of which act as cyclooxygenase (COX)-2 inhibitors. L-leucine methyl ester (Leu-OME) is a reagent which has been shown to kill phagocytes following interaction with intracellular proteases. There are two pathways whereby Leu-OME becomes cytotoxic to phagocytes. Within lysosomes, Leu-OME is converted into free Leu, which causes disruption of the lysosomes and subsequent cell necrosis. The other is the conversion of Leu-OME into (Leu-Leu)(n)-OME, which is associated with the induction of apoptosis. In the present study, we examined the action of T614 on Leu-OME mediated killing of THP-1, a human monocytic cell line. We revealed that T614 and phenylmethyl sulfonyl fluoride (PMSF), a serine protease inhibitor, inhibited Leu-OME mediated killing of THP-1 cells. All the other mNSAIDs, including nimesulide (NIM-03), fluosulide (CGP28238), FK3311 and NS398, also rescued THP-1 from Leu-OME mediated killing, although to a lesser degree. Of the classical NSAIDs tested, a protective effect was observed with diclofenac at high concentration, but not with naproxen or indomethacin. Unlike conventional lysosomal inhibitors, such as chloroquine and ammonium chloride (NH(4)Cl), T614 and PMSF did not raise lysosomal pH, as measured by flow cytometry using fluorescein isothiocyanate dextran (FITC-dextran). Therefore, the mechanism whereby T614 and PMSF inhibit Leu-OME killing is distinct from that of chloroquine or NH(4)Cl. Based on the similarity of T614 and PMSF, we suggest that, besides their roles as COX-2 inhibitors, T614 and other mNSAIDs may act as lysosomal protease inhibitors.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1986

Antigen presentation by human dermal fibroblasts: activation of resting T lymphocytes.

We have shown that human dermal fibroblasts, exposed to interferon-gamma (IFN-gamma) to induce surface class II major histocompatibility complex (MHC) antigens, were capable of presenting tetanus toxoid (TT) antigen to human TT-specific T cell clones. Antigen presentation by fibroblasts was antigen dependent, required HLA-DR expression by fibroblasts, and was MHC restricted. In contrast, we now report that IFN-gamma-treated fibroblasts are unable to present TT antigen to purified resting T cells obtained from the peripheral blood of TT-immune donors. In addition, although IFN-gamma-treated fibroblasts were able to stimulate alloreactive T cell clones, they were unable by themselves to stimulate primary allogeneic responses in resting T cells. The failure of fibroblasts to stimulate resting T cells was not due to suppressor effects by fibroblasts, because induction of TT and alloantigen responses in resting T cells by monocytes was not inhibited by the presence of fibroblasts. On the contrary, IFN-treated fibroblasts were synergistic with small numbers of monocytes in activating resting T cells. In addition, the failure of antigen presentation by fibroblasts to resting T cells was reversed by the addition of recombinant human interleukin 2 (rIL 2) to cultures, but not of purified human interleukin 1 (IL 1). These results emphasize that the requirements for activation of resting T cells differ from those of T cell clones. Although fibroblasts can efficiently present antigen to T cell clones, antigen presentation by fibroblasts to resting T cells requires the addition of exogenous IL 2. It is postulated that fibroblasts differ from classical antigen-presenting cells in that fibroblasts are incapable of stimulating the production of IL 2 in resting T cells.

Adult↗

PubMed1998

Neuroinvasion by ovine lentivirus in infected sheep mediated by inflammatory cells associated with experimental allergic encephalomyelitis.

Maedi Visna Virus (MVV) is a prototypic lentivirus that causes infection only in cells of macrophage lineage, unlike the primate lentiviruses which infect both CD4+ T lymphocytes and macrophages. In primates, the earliest viral invasion is associated with the ability of the virus to infect and activate T cells which convey virus to the brain. Infected monocytes in blood rarely cause CNS infection in absence of activation of CD4+ T cells. In the face of lack of infection or activation of T cells by MVV in sheep, the question arises, how does MVV gain access to the brain to cause the classical lesions of visna? In previous studies on experimental induction of visna, sheep were inoculated with virus directly in the brain. In this study, we asked whether neuroinvasion by MVV would occur if sheep were inoculated with virus in a non-neural site. Nine sheep were inoculated intratracheally and all developed systemic infection when examined 3 weeks later. At this time, five were injected intramuscularly with brain white matter homogenized in Freund's complete adjuvant to induce EAE. None of the four animals inoculated with virus alone developed CNS infection despite typical lentiviral infection in lungs, lymphoid tissues and blood-borne mononuclear cells. In contrast, all five of the sheep injected with brain homogenate developed infection in the brain. Virus was produced by macrophages associated with the EAE lesions. This study illustrated that both activated T cells specific for antigen in the CNS and infected macrophages are essential for lentivirus neuropathogenesis.

Animals↗

PubMed2002

Apoptosis of thymocytes related to cytokine expression in experimental classical swine fever.

Atrophy of the thymic cortex and loss of thymocytes were studied in 32 pigs inoculated with the virulent strain "Alfort" of classical swine fever (CSF) virus and killed at intervals from 2 to 15 days after infection. Immunohistochemical, ultrastructural, ELISA and TUNEL methods were used. The results suggested that direct action of CSF virus on thymocytes played no more than a minor role. The massive lymphoid depletion observed in the thymus, may, however, have been associated with the numerical increase in monocytes-macrophages in this organ, and their secretory activation, leading to synthesis and release of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1alpha and C1q complement component as main chemical mediators, and IL-1beta and IL-6 as minor mediators. These cytokines (TNF-alpha and IL-1alpha) may have played a role in the apoptosis of thymocytes, demonstrated by TUNEL and ultrastructural methods. The pathogenetic mechanism outlined may contribute to the lymphoid depletion observed in others organs in CSF and may explain the lymphopenia characteristic of the disease.

Animals↗

PubMed1986

TdT activity in acute myeloid leukemias defined by monoclonal antibodies.

Blast cells from eight out of 71 patients diagnosed with acute myeloid leukemia (AML) by morphological, cytochemical, and immunological criteria showed TdT activity. Their distribution according to the FAB classification was one M1, one M2, one M4, two M5a, one M5b, one M6, and one undifferentiated case. The TdT+ AML cases did not show major clinical and hematological differences when compared with the classical TdT- AML patients. Other phenotypical aberrations in the expression of membrane antigens, apart from the presence of nuclear TdT, were not observed in these TdT+ cases after study with a large panel of monoclonal antibodies. A higher incidence of TdT+ cases was found among the monocytic variants of AML (M4 and M5)--four cases--than in the granulocytic variants (M1, M2, and M3)--2 cases. These TdT+ cases should be distinguished from mixed leukemias by double labeling techniques, assessing in the TdT+ AML the coexpression of TdT and myeloid markers in individual cells as shown in four of our cases.

Adult↗

PubMedDate not supplied

Detection of a novel human class II HLA antigen.

Genetic, molecular and cellular analyses of the HLA-D region of the major histocompatability complex (MHC) in man have led to the definition of three different products. Two of these, DR and MB (the latter also known as DC (ref. 1) and LB-E (ref. 2)) are defined with serological reagents; the third, known as SB (ref. 3) and PL-3 (ref. 4) is defined with primed lymphocyte typing (PLT) cells. The classical features attributed to HLA-D region encoded (class II) molecules are that they are cell-surface dimers consisting of a structurally conserved alpha-chain noncovalently associated with a polymorphic beta-chain and that they are found primarily on B lymphocytes, some monocyte populations, endothelial and certain other cells. Using these criteria a monoclonal antibody, B7/21, was described as reactive with HLA-DR (ref. 7). We have now re-evaluated B7/21 antibody reactivity using mutant lymphoblastoid cell lines. It appears that this antibody does not react with the molecularly defined D region products described to date but instead, recognizes a class II antigen with distinctive molecular characteristics. We provisionally refer to this antigen as FA.

Antibodies, Monoclonal↗

PubMed2001

Cloning and characterization of Siglec-10, a novel sialic acid binding member of the Ig superfamily, from human dendritic cells.

The Siglecs (sialic acid-binding Ig-like lectins) are a subfamily of I-type lectins, which specifically recognize sialic acids. Nine members of the family have been identified thus far. We have obtained a novel cDNA clone from a human dendritic cell cDNA library encoding a protein with sequence and structural features of the Siglec family, hence designated as Siglec-10. The full-length Siglec-10 cDNA encodes a type 1 transmembrane protein containing four extracellular immunoglobulin-like domains, a transmembrane region, and a cytoplasmic tail with two classical immunoreceptor tyrosine-based inhibitory motifs. The N-terminal V-set Ig domain has most of the amino acid residues typical of the Siglecs. Siglec-10 shows the closest homology to Siglec-5 and Siglec-3/CD33. Various cells and cell lines including monocytes and dendritic cells express Siglec-10. High levels of mRNA expression were seen in peripheral blood leukocytes, spleen, and liver. When expressed on COS-7 cells, Siglec-10 was able to bind human red blood cells and soluble sialoglycoconjugates in a sialic acid-dependent manner. The identification of Siglec-10 as a new Siglec family member and its expression profile, together with its sialic acid-dependent binding capacity, suggest that it may be involved in cell-cell recognition by interacting with sialylated ligands expressed on specific cell populations.

Amino Acid Motifs↗

PubMedDate not supplied

[Initial results of the clinical use of the immunostimulant bestatin (3-amino-2-hydroxy-4-phenylbutyryl leucine) in patients with chronic polyarthritis].

We tested the efficacy of the immunomodulator Bestatin, which has been successfully applied in Japan, in a preliminary open study in ten patients with classical or definite rheumatoid arthritis. Patients whose arthritis was characterized by a low humoral activity showed a partial remission of the disease after six months' application of increasing doses of 10-60 mg in 48 hours. We found a significant increase in superoxide release from peripheral monocytes. Humoral parameters of inflammation such as erythrocyte sedimentation rate, C3a complement fraction, prostaglandin E2, and thromboxane B2 decreased. Concerning the subpopulations of lymphocytes we found a slight increase of activated T-lymphocytes and a decrease of O-cells and B-cells. The T-helper/T-suppressor ratio remained unchanged. The rheumatoid factor and the antinuclear antibodies showed no alteration under the treatment. Two weeks after withdrawal of Bestatin the improvement of the clinical and humoral parameter of the inflammation in rheumatoid arthritis vanished. No serious side effects were seen. Our results contribute to a long-term controlled study of the immunomodulator Bestatin as basic drug in the treatment of rheumatoid arthritis.

Adjuvants, Immunologic↗

PubMed1995

Alterations and pathology of thalassemic red cells: comparison between alpha- and beta-thalassemia.

Two main types of thalassemia have been categorized according to defective production of the globin gene ie alpha-thalassemia and beta-thalassemia. We report different red cell abnormalities between these two types. The study included 139 thalassemic patients including 91 patients with hemoglobin (Hb) H disease (52 cases with the classical genotype and 39 cases with Hb Constant Spring) and 48 were beta-thalassemia/Hb E disease. The deformability index of thalassemic red cells measured by laser diffractometer was significantly lower than that of normal red cells. Increased susceptibility of the thalassemic red cells to monocyte phagocytosis was markedly noted. Few sialic acid molecules were scattered on red cell surface of thalassemic red cells. Reticulocytes with delayed maturation stage were also observed in thalassemia indicating enhanced release from the bone marrow. The alpha-thalassemic red cells had relatively better deformability, increased susceptibility to phagocytosis, reduced sialic acid content and greater degree irregular distribution of sialic acid on red cell surface as compared to beta-thalassemic red cells. The alpha-type with hemoglobin Constant Spring (Hb CS) had increased percentage of reticulocyte and young reticulocyte (high fluorescent intensity) as compared to beta-thalassemic red cells. The different abnormalities between alpha- and beta-thalassemic red cells may lead to different mechanism of red cell destruction and different severity of the disease.

Erythrocyte Deformability↗