Evaluation of rice genotypes for brown planthopper (BPH) resistance using molecular markers and phenotypic methods

Twenty eight (28) rice genotypes were used to evaluate the genetic variability based on known BPH resistant loci spread through most of the genome (chromosomes 2, 3, 4, 5, 6, 8, 10, 11 and 12), using closely linked simple sequence repeat (SSR) markers and by different phenotypic screening methods. A total number of 155 alleles were detected by 30 polymorphic markers with an average of 4.6 per locus. The genetic diversity, polymorphic information content (PIC) ranged from 0.15 to 0.89 and 0.13 to 0.88, respectively and the allele frequency ranged from 0.21 to 0.89. These microsatellite markers linked to BPH resistance loci classified rice genotypes into three clusters with additional sub groups and sub sub groups. Our study reveals high genetic variation and clear genotypic relationship for BPH resistance based on BPH resistance linked markers and known phenotypic screening methods such as standard seedbox screening technique, honey dew test and nymphal survival method. Phenotypic evaluation showed clear distinction between resistant and susceptible type by clearly revealing moderately resistant types as well. Combined use of phenotypic and genotypic evaluation methods can improve the efficiency of marker assisted selection and utilization of resistant genotypes for crop improvement by rice breeders.Keywords: Nilaparvata Lugens, microsatellite markers, polymorphism, genetic diversityAfrican Journal of Biotechnology Vol. 12(19), pp. 2515-252

Immune evasion in cancer: mechanistic basis and therapeutic strategies

Cancer immune evasion is a major stumbling block in designing effective anticancer therapeutic strategies. Although considerable progress has been made in understanding how cancers evade destructive immunity, measures to counteract tumor escape have not kept pace. There are a number of factors that contribute to tumor persistence despite having a normal host immune system. Immune editing is one of the key aspects why tumors evade surveillance causing the tumors to lie dormant in patients for years through “equilibrium” and “senescence” before re- emerging. In addition, tumors exploit several immunological processes such as targeting the regulatory T cell function or their secretions, antigen presentation, modifying the production of immune suppressive mediators, tolerance and immune deviation. Besides these, tumor heterogeneity and metastasis also play a critical role in tumor growth. A number of potential targets like promoting Th1, NK cell, γδ T cell responses, inhibiting Treg functionality, induction of IL-12, use of drugs including phytochemicals have been designed to counter tumor progression with much success. Some natural agents and phytochemicals merit further study. For example, use of certain key polysaccharide components from mushrooms and plants have shown possess therapeutic impact on tumor-imposed genetic instability, anti-growth signaling, replicative immortality, deregulated metabolism etc. In this review, we will discuss the advances made towards understanding the basis of cancer immune evasion and summarize the efficacy of various therapeutic measures and targets that have been developed or are being investigated to enhance tumor rejection

Characterization of a novel co-stimulatory molecule: a 155-160 kD B cell surface protein provides accessory help to CD4<SUP>+</SUP> T cells to proliferate and differentiate

Optimal activation of T cells to clonally expand requires at least two distinct biological signals; one is generated by the interaction of the T cell receptor (TcR) with peptides bound to MHC molecules. The other signal(s) is (are) generated by a functionally defined event called the co-stimulatory pathway. We have characterized the co-stimulatory property of a murine B lymphocyte membrane protein (155-160 kD) on resting CD4+ T cells. The study involved the isolation of a 155-160 kD protein (B1) from the membranes of LPS-stimulated B cells. When reconstituted into lipid vesicles, B1 exerted a dose-dependent proliferative response to CD4+ T cells, resulting in the predominant secretion of IL-4 and IL-5 after cross-linking receptors with anti-CD3 mAb. This protein is a phosphoglycoprotein which gives a single spot on two-dimensional gel electrophoresis under reducing conditions and as a distinct peak on reverse phase-HPLC. The B1 binds to the T cell surface as is demonstrated by electron microscopic autoradiography and scanning electron microscopy, as well as competitive binding assays. It does not cross-react with antibodies directed against ICAM-1, LFA-1 α, B7, HSA and VCAM-1, suggesting the novelty of the protein. Activation of CD4+ T cells with B1 in the presence of anti-CD3 resulted in the translocation of protein kinase C (PKC). The B1 is barely detectable on the surface of resting B cells and digestion of this protein with V8 protease and peptide N-glycosidase F resulted in distinct protein bands on an autoradiogram

Characterization of novel costimulatory molecules. A protien of 38-42 kDa from B cell surface is concerned with T cell activation and differentiation

Optimal activation of T cells often requires signals delivered by the ligation of T cell receptor (TcR) and those resulting from costimulatory interaction between certain T cell surface accessory molecules and their respective counter receptors on antigen presenting cells. The molecular events underlying the co-stimulatory activity are still not understood fully. Here we describe a 38-42-kDa (B3) protein, present on the surface of lipopolysaccharide-activated B cells, which can provide costimulation to resting T cells leading to a predominant release of interleukin (IL)-4 and IL-5 and negligible amounts of IL-2 and interferon-γ . Binding assay and electron microscopic autoradiography data suggest that this molecule binds T cells, and the same can be competed by unlabeled B3. Characterization experiments point out that B3 shows up as a single prominent peak on reverse phase-high performance liquid chromatography, runs as a single spot in reducing two-dimensional gel electrophoresis, and is a phosphoglycoprotein. The Western analysis indicate that it does not cross-react with antibodies directed against murine ICAM-1, LFA-1α , VCAM-1, HSA, and B7 suggesting the novelty of the protein. The internal amino acid sequence of this molecule suggests that it does not belong to a known category of murine B cell surface molecules

A 150-kDa molecule of macrophage membrane stimulates interleukin-2 and interferon-γ production and proliferation of ovalbumin-specific CD4<SUP>+</SUP> T cells

In the present study, we describe the potential co-stimulatory role of a macrophage membrane-associated protein of 150 kDa (M150). The protein was isolated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and was found to be a single molecule on two-dimensional gel electrophoresis. The molecule was re-constituted in phosphatidyl choline vesicles and tested for its ability to promote the proliferation and the secretion of lymphokines from T helper (Th) cells. The reconstituted M150 induced a significant proliferation of anti-CD3 monoclonal antibody (mAb)-stimulated ovalbumin-specific CD4<SUP>+</SUP> T cells. Further, Th cells activated with this molecule in the presence of anti-CD3 mAb mainly secreted interleukin (IL)-2 and interferon- but not IL-4. M150 could not promote the proliferation of Th cells, or lymphokine secretion in the absence of anti-CD3 mAb. These observations suggest that M150 acts by selectively activating a Th1-like immune response

Characterization of novel costimulatory molecules. A protein of 38-42 kDa from B cell surface is concerned with T cell activation and differentiation

Optimal activation of T cells often requires signals delivered by the ligation of T cell receptor (TcR) and those resulting from costimulatory interaction between certain T cell surface accessory molecules and their respective counter receptors on antigen presenting cells. The molecular events underlying the co-stimulatory activity are still not understood fully. Here we describe a 38-42-kDa (B3) protein, present on the surface of lipopolysaccharide-activated B cells, which can provide costimulation to resting T cells leading to a predominant release of interleukin (IL)-4 and IL-5 and negligible amounts of IL-2 and interferon-γ. Binding assay and electron microscopic autoradiography data suggest that this molecule binds T cells, and the same can be competed by unlabeled B3. Characterization experiments point out that B3 shows up as a single prominent peak on reverse phase-high performance liquid chromatography, runs as a single spot in reducing two-dimensional gel electrophoresis, and is a phosphoglycoprotein. The Western analysis indicate that it does not cross-react with antibodies directed against murine ICAM-1, LFA-1α , VCAM-1, HSA, and B7 suggesting the novelty of the protein. The internal amino acid sequence of this molecule suggests that it does not belong to a known category of murine B cell surface molecules

M150 modulates the costimulatory signals delivered by B cells to T cells and enhances their ability to help B cells

There is a prerequirement of at least two sets of signals delivered by the antigen-presenting cell (APC) for the optimal activation of T helper (Th) cells. The First signal is provided by the engagement of T cell receptor with the antigen-MHC class II complex, followed by a second stimulus in the form of costimulatory signals. In the present study, we provide evidence that in a T-dependent antigen-driven system, the signals generated by hapten-specific B cells to stimulate Th cells for the secretion of interleukin-2 (IL-2), interferon-γ (IFN-γ ), and IL-4 were differentially modified by M150, a 150-kDa molecule expressed on the surface of macrophages. When ovalbumin-specific Th cells were cultured in the presence of 2,4,6 trinitrophenol (TNP)-specific B cells, M150 significantly increased the proliferation of Th cells and the secretion of IL-2 and IFN- γ and decreased the production of IL-4. Further, Th cells stimulated with M150 acquired improved ability to help B cells, resulting in an increase in the number of antibody-secreting cells and in the production of TNP-specific IgG2a antibodies. M150 possibly promotes Th1-like cell activity, as evidenced by predominant secretion of IL-2, IFN-γ , and IgG2a but not IL-4 and IgG1