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A Juretić

Publications and source records attributed to A Juretić.

18 recordsLinked to original sources
PubMed2001

Alterations in lymphocyte phenotype of infected preterm newborns.

The cord blood lymphocytes from 44 premature newborns were analyzed using two-color monoclonal antibodies and flow cytometry. Depending on whether or not there was an infection at birth, the newborns were divided into two groups and the immunophenotypes of infected and uninfected newborns were compared. The percentage of T lymphocytes (CD3+) was significantly lower in the infected prematures. The percentage of both helper and cytotoxic T lymphocytes was lower. The proportion of activated T lymphocytes, cytotoxic non-MHC-restricted T lymphocytes, NK cells and B lymphocytes did not differ between the group of infected and the group of uninfected prematures. The percentage of memory helper T lymphocytes (CD45RO+CD4+) was very low in premature newborns regardless of whether or not they were infected and could not be used as a marker of bacterial infection at this age.

B-Lymphocytes↗
PubMed2001

RT-PCR detection of tyrosinase, gp100, MART1/Melan-A, and TRP-2 gene transcripts in peripheral blood of melanoma patients.

AIM: To detect the expression of genes encoding tyrosinase, gp100, MART-1/Melan A, and tyrosinase-related protein-2 (TRP-2) in peripheral blood of melanoma patients by reverse transcription-polymerase chain reaction (RT-PCR). METHODS: Nineteen peripheral blood samples were obtained from 17 melanoma patients. When tested, 15 of them presented with clinically detectable metastatic disease. Samples of peripheral blood (7 mL) were collected from each patient into vacutainer cell preparation tubes. Mononuclear cells were isolated, total cellular RNA extracted, and then used as a template for reverse transcription to complementary DNA (cDNA). The cDNA was thereafter assayed by PCR for the expression of melanocyte-associated transcripts of tyrosinase, gp100, MART1/Melan-A, and TRP-2 genes. RESULTS: Gp100 gene expression was detected in 13 out of 19 samples. In 4 of them, TRP-2 gene expression was also detectable. Expression of tyrosinase and Melan-A/MART-1 genes could not be observed. Interestingly, gp100 and TRP-2 gene transcripts were detected in patients having recurrent and/or metastatic disease at the time of testing. CONCLUSION: The results we obtained support the use of RT-PCR assay for indirect detection of melanoma cells in peripheral blood of melanoma patients. As the transcripts for the tyrosinase gene and MART-1/Melan A gene were not detected, additional optimization experiments of RT-PCR assay are required.

Adult↗
PubMed2000

Two-color flow cytometric analysis of preterm and term newborn lymphocytes.

Immune system maturation proceeds postnatally in humans. Therefore, newborns, especially those of a lower gestational age, are not fully immunocompetent and are more likely to acquire perinatal infections. In order to investigate the neonatal immune system status, the major lymphocyte subpopulations were studied in newborns of different gestational age, comparing term newborns and adults. The cord blood from 66 newborns and the peripheral blood from 23 adults were analyzed using fluorochrome labelled monoclonal antibodies and two-color flow cytometry. The newborns were divided into three groups according to their gestational age. Ten prematures were under 32 weeks of gestation, 35 were of 32-37 weeks and there were 21 term newborns. The percentage of cytotoxic T lymphocytes (CD4 CD8+) was lower in term newborns as compared to the adult controls (17.8 versus 30.3%), and so were the percentages of activated T lymphocytes (CD3+Ia+; 0.3 versus 3.7%), cytotoxic non-MHC restricted T lymphocytes (CD3+CD16+CD56+; 0.2 versus 1.8%) and NK cells (CD3-CD16+CD56+; 4.8 versus 15.5%). On the contrary, the proportions of unlabelled cells were increased in term cord blood. The expression of CD45R0 marker on neonatal lymphocytes was very low (1%). In comparison to the higher-gestation newborns, the lower gestation prematures had reduced percentages of T lymphocytes (CD3+; 43 versus 65%), mostly helper T lymphocytes (CD4+CD8-; 35 versus 50%), and increased percentages of unlabelled cells. The percentages of NK cells (CD3+CD16+CD56+) and B lymphocytes (CD3-CD19+; CD3-Ia+) did not differ among the tested newborn groups. There were no significant differences in major lymphocyte subpopulations between the group of highest-gestation prematures and the group of term newborns that differed significantly when compared to adults. The lowest-gestation newborns showed the most immature lymphocyte phenotype with the highest percentages of unlabelled cells.

Antigens, CD19↗
PubMed1996

Nitric oxide-independent inhibitory effects of L-arginine analog NG-monomethy-L-arginine on the generation of interleukin-2 activated cytotoxic activity in humans.

Nitric oxide (NO) derived intracellularly from L-arginine (Arg) is indispensable for optimalgeneration of lymphokine-activated killer (LAK) cell activity in rodents. Still unclear, however, is its role in humans. To address this question human peripheral blood mononuclear cells (PBMC) from healthy donors were cultured in L-arginine free medium supplemented with recombinant interleukin-2 (rIL-2) and in the presence of exogenous L-arginine analog NG-monomethyl-L-arginine (NMMA), a specific inhibitor of the NO synthetic pathway. Cultured PBMC were tested for cytotoxic activity, proliferative capacity, and expression of phenotypic and activation markers (CD3, CD4, CD8, CD16, CD56 and CD25). Culture supernatants were assayed for nitrite (NO2-) and tumor necrosis factor-alpha (TNF-alpha) production. We found that NMMA inhibits the generation of optimal LAK cell activity when no exogenous Arg is supplied. Similar effects were also observed on proliferation, expression of IL-2 receptor induced upon rIL-2 stimulation and on TNF-alpha production. Sodium nitroprusside (SNP), used as a source of exogenous NO could not overcome this effect of NMMA on LAK cell activity. NO2- production was virtually undetectable in culture supernatants. Thus, NMMA affects in an NO-independent manner rlL-2 induced LAK activity in human PBMC.

Journal Article↗
PubMed1986

Influence of the combination of intraperitoneal and footpad immunization on anti-H-Y immunological reactivity.

In the following work the influence of the combination of intraperitoneal (i.p.) and footpad (f.p.) immunization on anti-H-Y immunological responsiveness in female CBA mice is described. Immunological responsiveness was determined on the basis of rejection or non-rejection of syngeneic male skin grafts from previously immunized CBA females. It was determined that the rejection of grafts is influenced by the nature of the first contact with the antigen. For instance, if the first immunization is by i.p. injection and the remainder by f.p. injections, then there is no rejection of grafts, and vice versa, rejection of grafts occurs if the first immunization is by f.p. injection regardless of whether the remainder are given i.p. The results are discussed in the context of existing theories in order to explain specific immunological (non-)responsiveness.

Animals↗
PubMed1985

Helper effects required during in vivo priming for a cytolytic response to the H-Y antigen in nonresponder mice.

Induction of H-Y-specific cytotoxic T lymphocyte (CTL) responses in nonresponder female mice was attempted by i.v. injection of allogeneic male cells, followed by in vitro restimulation of recipient spleen cells with syngeneic male cells. Responses were obtained only in two strain combinations in which the recipients, although phenotypically nonresponders, carried responder alleles at class I major histocompatibility complex (MHC) loci, and the immunizing cells differed from the recipients at class II MHC loci. The two positive strain combinations were B10.A(2R) anti-B10.A(4R), and B10.GD anti-B10.D2(R101). In the first combination, both recipient and donor are nonresponders to H-Y, and the CTL are induced via a bystander effect of another CTL response to a previously undetected minor histocompatibility (H) antigen. This "carrier" antigen can only induce CTL against H-Y and itself when the immunizing cells express class II MHC molecules. Furthermore, the presence of H-Y and the carrier antigen on the same cell is a prerequisite for the generation of H-Y-specific CTL. In the second combination, the recipient is a nonresponder, whereas the donor is a responder. The two strains differ at only E alpha and E beta class II MHC loci. For the induction of CTL, H-Y and the foreign E molecule must be expressed on the same cells. Thus, the B10.D2(R101) cells that express E molecules on their surface probably provide the E-nonexpressor B10.GD recipients with a stimulus for the generation of H-Y-specific T helper cells. The data are consistent with the notion that antigen-specific class II MHC-restricted T helper cells are involved in the initiation of CTL responses to minor H antigens.

Animals↗
PubMed1985

Cytotoxic T-cell response to H-Y antigen by B6.C-H-2bm12 and B10.BR mice.

Cytotoxic T-cell response to the male-specific histocompatibility antigen (H-Y) is often used as an experimental model for studying the genetic control of the immune response. This anti-H-Y response is shown to be a complex one, with multicellular interactions involving genes of the H-2 complex, and also some genes unlinked to H-2. For the analysis of the genetic control of the anti-H-Y immune response, different inbred strains have been used and classified accordingly as responders or non-responders. During the authors' studies of the genetic control of the immune response, some of the strains described as non-responders were found to behave as responders, namely strains B6.C-H-2bm12 and B10.BR. This finding has added to the intricacy of current data on the genetic control of immune response to H-Y antigen.

Animals↗
PubMed1984

Qa-like genes defined by CTL analysis of B10.W lines.

Twelve responder-stimulator combinations of mouse B10.W strains identical at K, D, and class II loci were tested for the generation of cytolytic T lymphocytes (CTL). No primary CTL could be obtained in any of the combinations but in nine combinations CTL were generated after priming in vivo. Six of these CTL are described. They define five antigenic determinants expressed exclusively in a small group of B10.W lines. The determinants appear to be part of the same system that resembles the Qa system originally defined in classic inbred strains. This resemblance rests on the observation that in vivo priming is necessary for the generation of the CTL, and that the CTL are not restricted in their reactivity by known H-2 loci. At least some of the determinants, however, appear to be controlled by a locus (or loci) associated with the K-rather than the D-end of the H-2 complex. Furthermore, some of the CTL directed against these Qa-like determinants cross-react with a molecule controlled by the K locus.

Animals↗
PubMed1984

H-41, a new minor histocompatibility locus. I. Histogenetic analysis.

The B10.STA12 mouse congenic line inherited from the wild mouse parent not only the H-2w13 haplotype but also an allele at a minor H locus, which we designate H-41. This allele (H-41a) differentiates the B10.STA12 line from B10.STA10 and B10.LIB55, which carry identical H-2w13 haplotypes but a different H-41 allele (the H-41b, also present in the background strain C57BL/10Sn). The B10.STA12 and B10.STA10 lines reject each other's skin grafts and generate cytolytic T lymphocytes (CTL) after in vivo immunization and in vitro restimulation with cells of the partner strain. The B10.STA12 anti-B10.STA10 CTL react with B10.STA10, B10.LIB55, and B10.STA39 target cells and with cells of F1 hybrids between the responder strain B10.STA12 and strains C57BL/6, C57BL/10, C57L, BALB/c, A, AKR, WB, DBA/1, and DBA/2 but fail to react with (C3H x B10.STA12) F1 and (CBA x B10.STA12) F1 cells. The B10.STA10 anti-B10.STA12 CTL react with B10.STA12, B10.P, and C3H.NB cells but fail to react to (B6 x B10.STA10) F1 target cells. The CTL reactivity in both combinations is Dp restricted. The B10.STA10 anti-B10.STA12 CTL exhibit, in addition, a cross-reactivity with B10.SAA48 cells that may be directed at one of the alloantigens controlled by the H-2 haplotype of this strain.

Animals↗
PubMed1983

Residual minor histocompatibility genes contaminate the B10.AM congenic line: no evidence of C-region-controlled histoincompatibility.

After being primed in vivo and restimulated in vitro, cytolytic T lymphocytes (CTL) were produced in the strain combinations B10.AM anti-B10.A(1R) and B10.A(1R) anti-B10.AM. Although the two strains differ in the chromosomal interval between the E alpha and the D loci, the CTL are not directed against antigens controlled by loci in this interval. Instead, the CTL detect minor histocompatibility (H) antigens controlled by loci that are not linked to H-2. The recognition of the antigens detected by the B10.AM anti-B10.A(1R) CTL is restricted by the Kk and Db molecules, but the CTL also cross-react with the Dd molecule (or a molecule controlled by a locus closely linked to Dd). The recognition of the antigens detected by these two CTL behave as if controlled by alleles at the same minor H locus or loci. This locus is distinct from H-2, and the B10.AM congenic line apparently retained a C3H-derived allele at this locus.

Alleles↗
PubMed1982

Cytolytic T cells activated by H-2-controlled E molecules cross-react with A molecules.

Cell-mediated lymphocytotoxicity was generated in four strain combinations differing only by the cell-surface expression of the class II E molecule controlled by the H-2 complex. The four combinations were: B10.D2(R107) anti-B10.A(3R), B10.A(4R) anti-B10.A(2R), B10.GD anti-B10.D2(R101), and B10.S(7R) anti-B10.S(9R). In all four of these combinations, the stimulator expresses E molecules on the cell surface, while the responder does not. The cytolytic T lymphocytes generated in the B10.D2(R107) anti-B10.A(3R) and B10.A(4R) anti-B10.A(2R) combinations reacted not only with the stimulator but also with strains that do not express cell-surface E molecules, in particular, strains carrying the H-2f and H-2q haplotypes. The cross-reactivity with E-negative strains could be blocked by monoclonal antibodies specific for the Af or Aq molecules but not by antibodies recognizing determinants on E or class I (K) molecules. The anti-H-2f cross-reactivity could be inhibited by H-2q cold targets and, reciprocally, the anti-H-2q reactivity could be blocked by H-2f cold targets. These findings are interpreted as indicating that the cytolytic T lymphocytes stimulated by E molecules can recognize and lyse cells lacking E molecules but expressing A molecules. The observed E-A cross-reactivity supports the notion of structural and functional relatedness between the A and E molecules and suggests a common evolutionary origin of the A- and E-encoding loci.

Animals↗
PubMed1981

Detection of CML determinants associated with H-2 controlled E beta and E alpha chains.

The serologically detectable molecules encoded by the H-2 complex, the major histocompatibility complex (MHC) of the mouse, fall into two classes-class I and class II (ref. 1). The class I molecules encoded by the K and D loci have a molecular weight of 44,000 and are noncovalently associated with beta 2 microglobulin which is not controlled by the MHC. The class II molecules are of two kinds, A and E, each consisting of two noncovalently associated polypeptide chains, alpha (Mr approximately 34,000) and beta (Mr approximately 28,000). Three of the four chains, A alpha, A beta and E beta, are controlled by loci in the I-A subregion, whereas the locus controlling the E alpha chain is located in the I-E subregion of the H-2 complex. Thus the loci coding for the E alpha and E beta chains are separated by at least one (J) and perhaps more loci. It has been shown that the E alpha and E beta chains are synthesized independently, and that the E alpha chain is required for the insertion of the E beta chain in the plasma membrane. We demonstrate here that the E alpha E beta complex (the E molecule) can evoke in vitro cell-mediated lymphocytotoxicity (CML) without previous sensitization in vivo, and that the strong CML reactivity is directed against allele-specific determinants on the highly polymorphic E beta chain.

Alleles↗
PubMed1981

Generation of cytotoxic T lymphocytes by the H-2-encoded E molecules.

Primary CML was generated in strain combinations 4R anti-2R, R107 anti-3R, 7R anti-9R, and GD anti-R101-combinations differing only in the chromosomal interval between the I-A subregion and the Ss locus. No CML could be obtained in any of the reciprocal combinations of these strains. This unidirectionality of the CML reaction correlates with the expression or nonexpression of the E molecules encoded by this interval: the reaction occurred in combinations in which the responder strain lacked and the stimulator strain expressed the E molecules in the cell membrane. The CML reaction was positive when tested on LPS-stimulated blast cells but weak on Con A-stimulated blasts and negative on Ia-negative tumor cells. The reaction could partially be inhibited by monoclonal antibodies to the Ia.m7 determinant presumably carried gy the E alpha chain; it was not inhibited by monoclonal antibodies specific for Ia determinants carried by the A molecule. Cytotoxic lymphocytes specific for a particular combination of E beta and E alpha chains reacted with all cells expressing the particular E beta chain, no matter what the origin of the E alpha chain associated with the E beta chain was. Attempts to generate cytotoxic lymphocytes specifically reactive with allotypic determinants on E alpha chains failed. In F1 hybrids expressing one type of E alpha chain and two types of E beta chain, the single E alpha chain was found to associate with both beta chains, producing two types of E molecule. We conclude from these experiments that the CML determinants detected in the strain combinations used are encoded by the same loci as those coding for the serologically detectable Ia determinants. The CML determinants are carried by the E beta chains; the E alpha chain does not contribute in any way to the specificity of determinant recognition by the cytotoxic lymphocytes. No evidence for allotypic variation of the E alpha chain as detected by the CML assay could be found in this study.

Animals↗
PubMedDate not supplied

[Radiotherapy of lung cancer].

The paper is aimed at approaching radiation therapy methods to physicians of other specialties and pointing to the potential of radiation therapy in the management of lung cancer patients. With the reference to its incidence and mortality rates, lung cancer ranks among the most frequent human malignant tumors. Therapy procedures for lung cancer depend upon tumor histology type, stage of disease and patient general condition. The said parameters therefore determine the application of surgery, radiation therapy and/or chemotherapy. In general, treatment results are usually rather poor, primarily due to lung cancer being the most frequently detected only as locally advanced or metastatic disease. Alike surgery, radiotherapy is a local form of treatment aimed at achieving local tumor control. This curative or palliative form of treatment is either applied alone or in combination with other treatment modalities. Irradiation is usually delivered by high energy photon beams from a telecobalt device or linear accelerator. The success of radiation therapy complies with the irradiation dose managed to be applied to tumor or tumor bed, which depends on patients general condition and site, size and spread of tumor. Radiotherapy with curative intent is applied in stage I, II and III non-small cell lung cancer patients with surgery being primarily applied in those with stage I and II. The efficacy of surgical treatment is to be improved by a combined-modality treatment. In stage III patients, who are more frequent than others, radical radiotherapy alone or in combination with chemotherapy is applied. Results of clinical trials report patients of relatively good general condition benefiting from combined-modality therapy. Palliative radiotherapy is to be applied in patients with stage IV non-small cell lung cancer. On the other hand, in patients with small cell lung cancer chemotherapy is the primary modality treatment. When the disease is limited to the lungs, the aim of radiotherapy is to optimize local control of the primary tumor.

Combined Modality Therapy↗
PubMedDate not supplied

[Radiotherapy treatment of lymphoma].

Radiotherapy and/or chemotherapy are primary treatment modalities in the therapy of lymphoma. The treatment depends on the lymphoma type, stage of disease and patients general condition. Radiation therapy is applied with curative or palliative intent, either as a single or combined modality treatment. In patients with stage I and stage IIA Hodgkin's lymphoma (HL) and no adverse risk factors, radiotherapy is applied as a single modality treatment. Moreover, treatment modalities in early-stage HL (I and IIA) consisting of either chemotherapy alone or combined with radiotherapy are the subject of ongoing clinical trials. In addition to the region/s with clinically involved lymph nodes, the target volume of radiation therapy applied as a primary radical treatment modality (stages I and IIA) also includes non-involved lymph nodes of adjacent regions aimed at their prophylactic irradiation. Such extended radiation fields are, for instance, the "mantle-field" and the "inverted-Y" field. On the other hand, with radiation therapy applied in combination with chemotherapy, the target volume depends on both the stage of the disease and the number of chemotherapy cycles. Likewise, the combined treatment is dependent on whether the role of radiotherapy is only the control of clinically involved regions, or of regions with potential subclinical disease too. Chemotherapy is the most frequently applied treatment modality in the management of non-Hodgkin's lymphoma (NHL). Radiation therapy as a single modality treatment with curative intent is applied in patients with, according to the histopathologic classification of the disease, the indolent NHL type and pathological stages I and II in continuation. The target radiation volume includes the clinically involved region, and possibly other adjacent clinically non-involved regions. In higher stages of disease or other, more aggressive NHL chemotherapy is applied either alone or in combination with adjuvant radiotherapy.

Hodgkin Disease↗