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PubMed1992

Inconsistency of the immunophenotype of Reed-Sternberg cells in simultaneous and consecutive specimens from the same patients. A paraffin section evaluation in 56 patients.

Both immunophenotypic overlaps between Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL), and evolution of one into the other have been reported. However, the underlying assumption that the antigenic expression of Reed-Sternberg (RS) cells is consistent in the same patient has not been evaluated. Such an evaluation was undertaken by immunophenotyping paraffin-embedded lymphoid tissue biopsies with HD from 56 patients in whom multiple specimens were obtained, either simultaneously from different sites or at different times. The panel of antibodies we used included: CD3 polyclonal antiserum, DAKO-M1 (CD15), L26 (CD20), BerH2 (CD30), MT1 (CD43), DAKO-LCA (CD45RB), UCHL1 (CD45R0), LN2 (CD74), and DAKO-EMA. The phenotype of RS cells was identical in simultaneous biopsies in only 11 of 39 patients (28%) and remained constant in consecutive biopsies in only 4 of 21 patients (19%). Major differences (relative to cell lineage specific antigens) were observed in 10 of 39 patients with simultaneous biopsies and in 10 of 21 patients over time; they mainly involved expression of T-cell antigens. Minor differences (relative to any other antigen) were observed in 22 of 39 patients with simultaneous biopsies and in 15 of 21 patients over time; these mainly involved CD15 or CD74. This striking variability of the immunophenotype of RS cells in the same patient may be due to aberrant marker expression, as a result of the neoplastic state, and/or to modulation of antigenic expression in relation to the host environment. This inconsistency suggests caution when interpreting the relationship between HD and NHL by paraffin immunophenotyping alone.

Antibodies↗
PubMed1999

Cytotoxicity with Auger electron-emitting radionuclides delivered by antibodies.

We investigated the in vitro cytotoxic potential of Auger electron-emitting radionuclides delivered to the cytoplasm or, more specifically, to lysosomes, via antibodies. The antibody (Ab) used was LL1, which is specific for CD74, an epitope of the major histocompatibility complex (MHC) class II antigen invariant chain, Ii, present on the cell surface. It is taken up in large amounts, approximately 10(7) Ab molecules per cell per day, and delivered to lysosomes. The radioisotopes tested included (111)In, 99mTc and 125I. With sufficient specific activity, approximately 10 mCi/mg Ab, all of these isotopes were potent cytotoxic agents. 125I was active only if a "residualizing" form was used, meaning a form that is trapped within cells after catabolism of the Ab to which it was conjugated (conventional oxidative iodination produces a non-residualizing label). The conjugates of (111)In and 99mTc used are known to be residualizing. One hundred percent cell kill in vitro was obtained with (111)In and 125I, under conditions in which a non-reactive control Ab, conjugated in the same way, produced no significant toxicity. 99mTc was also potent and specific, but appeared somewhat less active than the other isotopes under the conditions evaluated. Although few Abs are accreted by cells at the same rate as LL1, it may be possible to use other Abs to deliver similar amounts of radioactivity, if Abs with higher specific activity can be produced. Such conjugated radioisotopes may be useful for attacking tumor cells in vivo, particularly for single cells or micrometastases.

Antibodies↗
PubMed1999

Characterization of cellular response to thiol-modified gold surfaces implanted in mouse peritoneal cavity.

The early inflammatory reaction in vivo to three well defined surfaces-gold, gold coated with glutathione (GSH), and 3-mercapto-1, 2-propanediol (MG)-was assessed as manifested by the adherence and activation of inflammatory cells during implantation intraperitoneally in mice. Evaluation of cell adhesion and activation was done by immunohistochemistry using specific monoclonal antibodies directed against cell differentiation antigens CD11b/CD18, CD74, and CD25 or by measurement by chemoluminescence of reactive oxygen radical species produced by adhering cells. Cell recruitment and activation was slow on the GSH-coated gold surfaces. These surfaces also had the highest percentage of adhering cells with an intact cell membrane. The MG-coated surfaces, on the other hand, rapidly recruited and activated cells and also caused cell membrane leakage to propidium iodide, suggesting cell membrane damage or cell death. The respiratory burst of adhering cells was stimulated by phorbol-myristate acetate on the GSH-coated surface but not on the MG-coated surface and by opsonized zymosan on the Mg-coated surface but only to a small degree on the GSH-coated surface. The respiratory burst following zymosan activation of cells adhering to the MG-coated surface was inhibited by treatment with 2. 3-diphosphoglycerate, a phospholipase D inhibitor. The presented data suggest that peritoneal leukocytes adhering to foreign materials may raise a respiratory burst response via a phospholipase D-dependent and protein kinase C-independent pathway.

Animals↗
PubMed1990

Histopathologic, immunophenotypic, and genotypic analysis of Ki-1 anaplastic large cell lymphomas that express histiocyte-associated antigens.

CD30/Ki-1 antigen expression in 243 cases of malignant lymphomas was examined using Ber-H2 monoclonal antibody. Among them 20 cases were categorized as Ki-1 anaplastic large cell lymphoma. In two of these cases histiocyte-associated markers were also expressed. In these cases histopathologic and extensive in situ immunophenotypic analyses were used with genotypic studies in the determination of cell lineage. A sinusoid histologic pattern of involvement with partial lymph node infiltration by pleomorphic neoplastic cells was noticed in the nodes from both patients. Solid areas of node replacement resembling metastatic carcinoma were seen in Patient 1. Immunohistologically, tumor cells of both cases were positive for CD30, CD25, CD71, LN3 (HLA-DR), EMA, CD45, CD74, vimentin, alpha-1-antichymotrypsin, and CD68. Patient 1 was also CD45RO+, CD43+, whereas Patient 2 was positive for alpha-1-antitrypsin and CD4 tumor cells. Genotypic studies revealed that TCR beta and TCR gamma chain genes were clonally rearranged in Patient 1, whereas no rearrangements were detected in Patient 2. This study supports the view that some Ki-1 anaplastic large cell lymphomas may express multiple histiocyte-associated antigens and confirms that this group of neoplasms have immunophenotypic heterogeneity. The results of genotypic analyses used with immunophenotyping does not exclude that the tumor cells in these cases may be of true histiocytic origin despite the Ki-1-positive phenotype.

Adolescent↗
PubMed1991

Primary cutaneous B-cell lymphoma: a unique type of low-grade lymphoma. Clinicopathologic and immunologic study of 83 cases.

The clinical presentation and course, and the morphoimmunologic features of primary cutaneous B-cell lymphoma (CBCL) were investigated in a series of 83 patients. Fifty-one patients were male and 32 were female (male-to-female ratio of 1.6:1); CBCL primarily involved the elderly (median age, 58 years). A locoregional extension of the disease was quite frequent (86.7%). The neoplastic cells showed a range of appearances reminiscent of the whole spectrum of follicular/parafollicular cells. The antigenic phenotype of tumor cells (CD19+, CD20+, CD22+, CD28+, CD10-, CD5-, MB2+, CD74+/-, CDw75+/-, MT2+/-, surface immunoglobulin + monoclonal/-) plus the presence of admixed CD14- dendritic reticulum cells suggest a mantle-zone nature for CBCL. The nonaggressive clinical behavior with a substantial tendency to remain localized to a limited area of the skin, the quite good response to nonaggressive treatment, and the dichotomy existing between the enhancement of morphoimmunologic atypism--which parallels the increasing age and growth rate of lesions--and the constant benign overall prognosis on long-term follow-up make CBCL a unique type of lymphoma of low-grade malignancy. Proper recognition of CBCL is mandatory to avoid possible undertreatment or overtreatment of the patients affected.

Adult↗
PubMed1992

CD30 (Ki-1)-positive, anaplastic large cell lymphoma mimicking gastrointestinal carcinoma.

BACKGROUND: There is great diversity in the clinical presentation of CD30 (Ki-1)-positive, anaplastic large cell lymphoma (ALCL). The authors report two patients in whom the clinical and morphologic features mimicked gastrointestinal carcinoma. METHODS: Surgical pathology specimens were examined using standard histologic techniques. Paraffin- and frozen-section immunohistochemistry was performed by an avidin-biotin-peroxidase method. RESULTS: The first patient is a 58-year-old man who presented with a constricting mass of the sigmoid colon. Immunohistochemical staining for CD45 (LCA) was negative in formalin-fixed paraffin sections. However, CD45 and CD74 (LN2) were detectable in B5 postfixed material. The second patient is a 44-year-old woman who presented with dysphagia and back pain. Endoscopic examination revealed an ulcerated luminal mass in the proximal esophagus and a gastric ulcer. Mucosal biopsy specimens of the esophagus and stomach contained ALCL, which was CD45 positive. Retroperitoneal lymph nodes contained ALCL infiltrating the sinuses, interfollicular areas, and blood vessel lumina. In addition to CD45 and pan-T-cell antigens, the neoplastic cells expressed CD68 (KP1) and epithelial membrane antigen (EMA). Monoclonal antikeratins were negative, but a polyclonal antikeratin stain was positive. CONCLUSIONS: These findings indicate that clinical, morphologic, and some immunologic features of ALCL may mimic gastrointestinal carcinoma.

Adult↗
PubMed1993

Specific skin manifestations in acute leukemia with monocytic differentiation. A morphologic and immunohistochemical study of 11 cases.

BACKGROUND: Monocytic differentiation is present in the myelomonocytic (M4) and monocytic (M5) type of acute myeloblastic leukemia. Infiltration of the skin in acute myelomonocytic leukemia occurs in 10-20% of patients, the skin lesions occasionally being the first symptom, even preceding monocytosis. METHODS: Eleven patients with myelomonocytic (n = 2) and monocytic leukemia (n = 9) were studied who had skin manifestations. RESULTS AND CONCLUSIONS: Clinically, all patients showed disseminated papules or nodules that corresponded histologically to nodular or diffuse infiltrates of monocytoid cells, occasionally displaying a whorled pattern. The currently available antibodies for paraffin-embedded sections (lysozyme, elastase, leukocyte common antigen (CD45), MT1 (CD43), Leu-M1 (CD15), LN2 (CD74), MB2, MB1 (CD45RA), LN1 (w75), Mac387, L26 (CD20), UCHL1 (CDR0), MT2 (CD45RA), and KP-1 (CD68)) and chloracetate-esterase are not more helpful in diagnosis than are the histologic findings. By contrast, the antibodies used on frozen sections (Leu-4 (CD3), Leu-3a (CD4), BA1 (CD24), B4 (CD19), Leu-M5 (CD11c), Vim12 (CD11b), VimD5 (CD15), KiM6 (CD68), KIM7 (CD68), My7 (CD13), and My9 (CD33) allow the definition of a reaction pattern that is diagnostic for acute myeloid leukemia with monocytic differentiation.

Adult↗
PubMed2025

Genetic Architecture of Idiopathic Inflammatory Myopathies From Meta-Analyses.

OBJECTIVE: Idiopathic inflammatory myopathies (IIMs, myositis) are rare systemic autoimmune disorders that lead to muscle inflammation, weakness, and extramuscular manifestations, with a strong genetic component influencing disease development and progression. Previous genome-wide association studies identified loci associated with IIMs. In this study, we imputed data from two prior genome-wide myositis studies and analyzed the largest myositis data set to date to identify novel risk loci and susceptibility genes associated with IIMs and its clinical subtypes. METHODS: We performed association analyses on 14,903 individuals (3,206 patients and 11,697 controls) with genotypes and imputed data from the Trans-Omics for Precision Medicine reference panel. Fine-mapping and expression quantitative trait locus colocalization analyses in myositis-relevant tissues indicated potential causal variants. Functional annotation and network analyses using the random walk with restart (RWR) algorithm explored underlying genetic networks and drug repurposing opportunities. RESULTS: Our analyses identified novel risk loci and susceptibility genes, such as FCRLA, NFKB1, IRF4, DCAKD, and ATXN2 in overall IIMs; NEMP2 in polymyositis; ACBC11 in dermatomyositis; and PSD3 in myositis with anti-histidyl-transfer RNA synthetase autoantibodies (anti-Jo-1). We also characterized effects of HLA region variants and the role of C4. Colocalization analyses suggested putative causal variants in DCAKD in skin and muscle, HCP5 in lung, and IRF4 in Epstein-Barr virus (EBV)-transformed lymphocytes, lung, and whole blood. RWR further prioritized additional candidate genes, including APP, CD74, CIITA, NR1H4, and TXNIP, for future investigation. CONCLUSION: Our study uncovers novel genetic regions contributing to IIMs, advancing our understanding of myositis pathogenesis and offering new insights for future research.

Humans↗
PubMed1994

Production of two monoclonal antibodies (FB1 and FB21) useful for the identification of human B lymphocytes in formalin-fixed, paraffin-embedded tissues.

Two monoclonal antibodies (FB1 and FB21) reactive in formalin-fixed, paraffin-embedded tissue sections are reported in this paper. FB1 and FB21 recognize a cytoplasmic antigen and a surface antigen of B cells, respectively. FB1 reacts with mantle zone (MZ) B cells, germinal centre (GC) cells, and marginal zone (MrZ) B cells, but not with T cells in lymphoid tissues. FB21 reacts with MZ B cells, GC cells in lymphoid tissues, and T cells of peripheral blood, but not with MrZ B cells in the spleen. Neither monoclonal antibody (MoAb) reacts with monocytes, granulocytes, or plasma cells. FB1 reacted with all the B-cell lymphomas tested and with CD20-positive Reed-Sternberg cells in two of five cases of Hodgkin's disease, but not with multiple myelomas or T-cell lymphomas. FB21 reacted with B-cell lymphoma in 20 of 22 cases, but not with multiple myelomas, T-cell lymphomas, or Reed-Sternberg cells of Hodgkin's disease. Immunoprecipitation studies revealed that FB1 recognizes the same two polypeptide chains that are recognized by L26 and is a member of the CD20 antibody cluster. FB21 was thought to recognize a sialic acid-dependent carbohydrate epitope and this was confirmed at the Fifth International Conference on Human Leukocyte Differentiation Antigens (Boston, 1993). FB21 did not react with splenic MrZ B cells and was different from the pan B markers reported previously [CD20 (L26), CD45RA (MB1), and CD74 (LN-2)]. FB21 recognizes a subset of B cells and appears to be closely related to CD75/76 antibodies. FB1 and FB21 are useful MoAbs for the diagnosis and analysis of B-cell lymphomas.

Animals↗
PubMed1996

Primary hepatic marginal zone B-cell lymphoma with mantle cell lymphoma phenotype.

We report a rare case of primary hepatic lymphoma, Stage II disease, in a 48-year-old male who had a solitary hepatic tumour measuring 4 x 4.5 x 3 cm. The tumour showed a nodular growth pattern and lymphoepithelial lesions with bile ducts. Some neoplastic nodules had a non-neoplastic atrophic germinal centre and/or a thin mantle cell layer. Morphologically, the neoplastic cells were centrocyte-like cells or intermediate lymphocytes. They expressed L26(CD20)+/LN-1(CDw75)+/-/LN-2(CD74)+/cyclin D1- and had a monotypic immunoglobulin of cytoplasmic IgM (kappa) on paraffin sections. The neoplastic cells or neoplastic nodules expressed surface IgM+/surface IgD+/-/Leu-1(CD5)+/DRC-1+/alkaline phosphatase+/B1(CD20)+/B4(CD19)- on fresh frozen sections. We therefore diagnosed this case as primary hepatic marginal zone B-cell lymphoma with mantle cell lymphoma phenotype. We confirm that it is difficult to differentiate extranodal marginal zone B-cell lymphoma (low grade B-cell lymphoma of mucosa-associated lymphoid tissue type; MALT lymphoma) and mantle cell lymphoma.

Biopsy, Needle↗
PubMed2006

Genomics of renal cell cancer-- does it provide breakthrough?

It is a strong hope that the more we characterize the pathways in an individual tumor, the better we will be able to evaluate the response to a specific therapy. Different array technologies could be powerful tools to achieve this goal, i.e. selecting patients on the basis of the genomic and/or proteomic profiles who would really benefit from the target-designed therapy. Genomic analysis of RCC accumulated ample of data which now can be exploited in clinical management of a previously almost uncontrollable disease. Beside the previously identified genetic abnormalities (VHL, MET, EGFR), CAIX seems to be a novel molecular marker of RCC. Array studies also outlined a small set of tumor markers, vimentin, galectin-3, CD74 and parvalbumin, which can define the individual histologic subtypes of RCC. We are at the beginning to take advantage of the genomic results. Some new approaches will interfere with the progression of RCC (anti-VEGF, anti-VEGFR or anti-EGFR therapies). Further novel molecular targets are available, such as HIF, HSP90 or the IFN-regulated genes, which can be used to the fine-tuning of RCC therapy.

Biomarkers, Tumor↗
PubMed1998

HLA-DM is expressed on the cell surface and colocalizes with HLA-DR and invariant chain in human Langerhans cells.

The subcellular distribution patterns of molecules involved in the process of antigen loading [HLA-DR, HLA-DM, and the cytoplasmic and luminal parts of the invariant chain (Ii, CD74)] were investigated in Langerhans cells (LC), both qualitatively and quantitatively. The analysis was performed by immunofluorescence labelling of acetone-fixed vertical cryostat sections from normal human skin specimens and subsequent examination using confocal laser scanning microscopy (CSLM). The intensity-modulated multiple-wavelength scanning (IMS) technique was used to enhance channel separation when scanning dual-labelled specimens. The mean (n = 9) relative epidermal volumes of reactivity were: HLA-DR 8%+/-3%, HLA-DM 6%+/-2%, luminal Ii 6%+/-2%, and cytoplasmic Ii 4%+/-1%. The difference between HLA-DR and the other epitopes was significant at the P<0.001 level. All molecule combinations, except the combination of HLA-DM and luminal Ii (which was not studied), were to various extents colocalized. Experiments performed on unfixed epidermal sheets showed that HLA-DM is present on the cell surface of LC, suggesting that HLA-DM may interact with HLA-DR on the surface to induce peptide loading.

Adult↗
PubMed2006

Antimicrobial peptides are present in immune and host defense cells of the human respiratory and gastrointestinal tracts.

Previous studies have implicated antimicrobial peptides in the host defense of the mammalian intestinal and respiratory tract. The aim of the present study has been to characterize further the expression of these molecules in non-epithelial cells of the human pulmonary and digestive systems by detailed immunohistochemical analysis of the small and large bowel and of the large airways and lung parenchyma. Additionally, cells obtained from bronchoalveolar lavage were analyzed by fluorescent activated cell sorting and immunostaining of cytospin preparations. hBD-1, hBD-2, and LL-37 were detected in lymphocytes and macrophages in the large airways, lung parenchyma, duodenum, and colon. Lymphocytes positive for the peptides revealed a staining pattern and distribution that largely matched that of CD3-positive and CD8-positive T-cells. Macrophages with positive staining for the antimicrobial peptides also stained positively for CD68 and CD74. In view of the morphology of the LL-37-positive and hBD-2-positive mucosal lymphocytes, they are probably also B-cells. Thus, antimicrobial peptides of the defensin and cathelicidin families are present in a variety of non-epithelial cells of mucosal organs. These findings confirm that antimicrobial peptides have multiple functions in the biology of the mucosa of these organs.

Antimicrobial Cationic Peptides↗
PubMed1992

B-zone small lymphocytic lymphoma: a morphologic, immunophenotypic, and clinical study with comparison to "well-differentiated" lymphocytic disorders.

The pathologic, immunologic, and clinical features of five cases of B-zone small lymphocytic lymphoma (BZSLL), characterized by a nondestructive growth pattern with a selective and complete replacement of the B-zone areas of lymph nodes, were examined. These findings were compared with those of 13 cases of intermediate differentiated lymphoma/mantle zone lymphoma (ILL/MZL) and 20 cases of typical small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL). B-zone SLL was characterized histologically by a deceptively benign pattern at a low magnification, the lymph node architecture being substantially preserved, in contrast to the ILL/MZL and SLL/CLL cases, in which complete effacement of the normal architecture usually could be observed. Moreover, in BZSLL the cellular population was rather uniform and lacked either a prolymphocytic component or the small-cleaved lymphoid cells often seen in SLL/CLL and ILL/MZL cases, respectively. The phenotypic profile of the BZSLL clonal cell population studied by the immunoperoxidase method and by single- and double-labeling flow cytometric analyses (SIg+, CD19+, CD20+, CD21+, CD22+, CD24+, CD35+, CD37+, CD74+, CD45+, CD45R+, MB2+, HLA-DR+, Leu-8+, CD9+/-, CDw75+/-, CD5-/+, CD23-/+, CD10-, FMC7-, PCA-1-, CD25-, CD38-, CD43-, CD3-) appeared to be fairly homogeneous and sufficiently distinct from that of ILL/MZL, based on the absence of FMC7 and CD38 molecules, and from that of SLL/CLL due to significantly stronger expression of SIgs (P less than .05), the higher reactivity with anti-CD9 and -CD22 antibodies (P less than .05), the lower reactivity with anti-CD5 and -CD23 antibodies (P less than .05), and the absence of CD25 determinants. Several clinical features of patients with BZSLL, including age group, advanced stage disease, and high frequency of bone marrow and peripheral blood involvement, were similar to those found in the other patients with ILL/MZL and SLL/CLL, but none of the BZSLL patients had an absolute lymphocyte count higher than 15.0 x 10(9)/L at presentation. Based on the architectural pattern, cytologic features, immunophenotypes, and hematologic findings, we conclude that BZSLL is an unusual variant of SLL that is primary in the lymph nodes and should be distinguished from ILL/MZL and CLL.

Adult↗
PubMed1992

Antigenic phenotypes of hairy cell leukemia and monocytoid B-cell lymphoma: an immunohistochemical evaluation of 66 cases.

Using a large panel of antibodies on multi-tumor block sections of routinely processed, paraffin-embedded fixed tissue, we compared the antigenic phenotype of 42 clinically, morphologically, and immunologically well-characterized cases of hairy cell leukemia (HCL) with 24 cases of monocytoid B-cell lymphoma (MBCL) selected from the Monocytoid B-Cell Lymphoma Registry at the City of Hope National Medical Center. The predominant antigenic phenotype of hairy cells was CD45 (leukocyte common antigen)+, CD45Ra (4KB5, MB1, MT2)+, L26+, CDw75 (LN1)+, CD74 (LN2)+, LN3+, MB2+, CD45RO (UCHL1)-, MT1-, CD15 (Leu-M1)-, neuron-specific enolase (NSE)-, epithelial membrane antigen-, and CD30 (Ber-H2)-. The immunophenotype of neoplastic monocytoid B lymphocytes was essentially identical to that of the hairy cells, with one exception: the neoplastic monocytoid B lymphocytes were stained by epithelial membrane antigen in seven cases. An interesting observation was the staining by anti-muscle-specific actin of the neoplastic cells of MBCL in 53% of cases, but of none of the cases of HCL. The results of our study (1) indicate that HCL and MBCL can be immunophenotyped reliably on fixed tissue samples, (2) further confirm the proposed lineage relationship between these two lymphoproliferative disorders, and (3) indicate that decalcification of bone marrow biopsies does not adversely affect the immunoreactivity of hematopoietic-associated antigens.

Antigens, Neoplasm↗
PubMed1992

Immunoarchitecture of normal human bone marrow: a study of frozen and fixed tissue sections.

To provide baseline information on the immunoarchitecture of normal bone marrow, we studied cryostat-cut, frozen, and paraffin-embedded, fixed tissue sections prepared from 21 core biopsies of normal bone marrow obtained during bone marrow harvests for transplantation. A large panel of antibodies was applied that included, for frozen tissue, Leu-6 (CD1), T11 (CD2), Leu-3a (CD4), Leu-1 (CD5), Leu-2a (CD8), J5 (CD10), My7 (CD13), Leu-11 (CD16), B4 (CD19), B1 (CD20), B2 (CD21), Tac (CD25), My9 (CD33), T200 (CD45), NKH-1 (CD56), kappa and lambda chains, beta F1, Ki-67, HLA-DR, TQ1, and keratin, and for fixed tissue, leukocyte common antigen (CD45), L26 (CD20), LN1 (CDw75), LN2 (CD74), LN3, LN4, LN5, MB1 (CD45R), MB2, MT1 (CD43), MT2 (CD45R), UCHL1 (CD45R0), BM1, Ki-1 (CD30), Leu-M1 (CD15), lysozyme, KP1 (CD68), actin, S100, neuron-specific enolase, vimentin, and keratin. On fresh-frozen sections CD19 and CD2 were the most reliable and sensitive markers for B and T cells, staining 5% and 9% of marrow cells, respectively. Immunoglobulins generally showed heavy background staining, which frequently precluded an accurate assessment. The CD4 to CD8 ratio in the bone marrow was reversed from that of peripheral blood. On fixed tissues, leukocyte common antigen was found in 14% of the marrow cells, corresponding roughly to the lymphocyte population. L26, a pan-B-cell marker, stained 3% of the marrow cells. Among the other B-cell markers, LN1 and MB2 stained a large number of cells (40% to 70%), indicating reactivity with cells of the myeloid or erythroid series in addition to lymphocytes. Among the T-cell markers, UCHL1 and MT1 stained 66% and 50% of the cells, respectively, which could be explained by their cross-reactivity with myeloid cells. Nonspecific myelomonocytic markers (Leu-M1, KP1, and lysozyme) also showed reactivity in a high percentage of cells. No particular architectural distribution patterns of B or T lymphocytes were noted in either frozen or fixed bone marrow specimens. The results of this study provide normal baseline data for the immunohistologic application of hematopoietic and lymphoid markers on frozen or fixed bone marrow biopsy specimens.

Adult↗
PubMed2005

Molecular markers distinguish bone marrow mesenchymal stem cells from fibroblasts.

To characterize mesenchymal stem cells (MSC), we compared gene expression profiles in human bone marrow MSC (11 lines) and human fibroblasts (4 lines) by RT-PCR and real time PCR. Messenger RNA levels of MHC-DR-alpha, MHC-DR-beta, MHC-DR-associated protein CD74, tissue factor pathway inhibitor-2, and neuroserpin were much higher in MSC than in fibroblasts, even in the presence of large interindividual variations. Those of adrenomedullin, apolipoprotein D, C-type lectin superfamily member-2, collagen type XV alpha1, CUG triplet repeat RNA-binding protein, matrix metalloproteinase-1, protein tyrosine kinase-7, and Sam68-like phosphotyrosine protein/T-STAR were lower in MSC than in fibroblasts. FACS analysis showed that cell surface expression of MHC-DR was also higher in MSC than in fibroblasts. MHC-DR expression decreased after osteogenic differentiation, whereas the expression of adrenomedullin-a potent stimulator of osteoblast activity-along with collagen XV alpha1 and apolipoprotein D increased after osteogenic differentiation. The marker genes identified in this study should be useful for characterization of MSC both in basic and clinical studies.

Biomarkers↗
PubMed2026

Proteomics combined with single-cell sequencing reveals key genes and computational lead compound related to ligamentum flavum hypertrophy, lactate metabolism and lactate modification.

Ligamentum flavum hypertrophy (LFH) is a hallmark pathological feature of lumbar spinal stenosis; however, its underlying molecular mechanisms remain incompletely understood. Lactate metabolism and related lactylation modifications have emerged as critical links between cellular metabolism and epigenetic regulation, with established roles in various fibrotic and inflammatory diseases. Nevertheless, the specific contribution of lactylation to LFH pathogenesis remains unexplored. In this study, we integrated proteomic profiling of ligamentum flavum tissues with single-cell transcriptomic data to identify differentially expressed proteins associated with LFH. Cross-referencing these genes with genes involved in lactate metabolism and lactylation yielded 16 candidate genes. Through functional enrichment analysis, protein-protein interaction network construction, and GraphBAN model prediction, we identified five hub genes (NDUFS2, HMOX1, SPR, FABP5, and PFKP) and two potential lead compounds (ZINC000014879975 and ZINC000242437513). Molecular docking analysis confirmed favorable binding affinities between these compounds, suggesting that they may serve as potential lead compounds worthy of further experimental investigation. Single-cell analysis further revealed that macrophages occupy a central position in the LFH microenvironment, resulting in pronounced metabolic reprogramming and remodeling of intercellular communication networks, particularly via the MIF-CD74/CD44 axis, under pathological conditions.

Proteomics↗