Differential Effect of B Lymphocyte–induced Maturation Protein (Blimp-1) Expression on Cell Fate during B Cell Development

The B lymphocyte–induced maturation protein (Blimp-1) upregulates the expression of syndecan-1 and J chain and represses that of c-myc. We have transfected Blimp-1 into two sublines of the BCL1 B cell lymphoma that represent distinct stages of B cell development in secondary lymphoid tissues. After interleukin (IL)-2 and IL-5 stimulation, the BCL1 3B3 cells differentiate into centrocyte-like cells, whereas the BCL1 5B1b cells blast and appear to be blocked at the centroblast stage. This blasting effect and the increase in IgM secretion that follows it can be blocked by a dominant negative form of Blimp-1. At the same time, the ectopic expression of Blimp-1 in these partially activated cells induces an apoptotic response that also can be suppressed by the same dominant negative protein. A similar effect was noticed when Blimp-1 was expressed in the mature L10A and the immature WEHI-231 lines, indicating this may be a general effect at earlier stages of the B cell development, and distinct from the ability of Blimp-1 to induce maturation in late stages of differentiation. Truncation mutants indicate that the induction of the apoptotic response relies mainly on 69 amino acids within Blimp-1''s proline-rich domain. We propose that Blimp-1 expression defines a checkpoint beyond which fully activated B cells proceed to the plasma cell stage, whereas immature and partially activated cells are eliminated at this point.     

The Molecular Mechanism of B Cell Activation by toll-like Receptor Protein RP-105

The B cell–specific transmembrane protein RP-105 belongs to the family of Drosophila toll-like proteins which are likely to trigger innate immune responses in mice and man. Here we demonstrate that the Src-family protein tyrosine kinase Lyn, protein kinase C β I/II (PKCβI/II), and Erk2-specific mitogen-activated protein (MAP) kinase kinase (MEK) are essential and probably functionally connected elements of the RP-105–mediated signaling cascade in B cells. We also find that negative regulation of RP-105–mediated activation of MAP kinases by membrane immunoglobulin may account for the phenomenon of antigen receptor–mediated arrest of RP-105–mediated B cell proliferation.     

Subunit Composition of Pre–T Cell Receptor Complexes Expressed by Primary Thymocytes: CD3δ Is Physically Associated but Not Functionally Required

Maturation of immature CD4⁻CD8⁻ (DN) thymocytes to the CD4⁺CD8⁺ (DP) stage of development is driven by signals transduced through a pre–T cell receptor (TCR) complex, whose hallmark is a novel subunit termed pre-Tα (pTα). However, the precise role of pre-TCRs in mediating the DN to DP transition remains unclear. Moreover, progress in understanding pre-TCR function has been hampered thus far because previous attempts to demonstrate expression of pTα-containing pre-TCRs on the surface of normal thymocytes have been unsuccessful. In this report, we demonstrate for the first time that pTα-containing pre-TCR complexes are expressed at low levels on the surface of primary thymocytes and that these pre-TCR complexes comprise a disulfide-linked pTα–TCR-β heterodimer associated not only with CD3-γ and -ε, as previously reported, but also with ζ and δ. Interestingly, while CD3-δ is associated with the pre-TCR complex, it is not required for pre-TCR function, as evidenced by the generation of normal numbers of DP thymocytes in CD3-δ–deficient mice. The fact that any of the signaling components of the pre-TCR are dispensable for pre-TCR function is indeed surprising, given that few pre-TCR complexes are actually expressed on the surface of primary thymocytes in vivo. Thus, pre-TCRs do not require the full array of TCR-associated signaling subunits (γ, δ, ε, and ζ), possibly because pTα itself possesses signaling capabilities.     

CD4+ T Cell–mediated Granulomatous Pathology in Schistosomiasis Is Downregulated by a B Cell–dependent Mechanism Requiring Fc Receptor Signaling

The effector functions of CD4⁺ T lymphocytes are generally thought to be controlled by distinct populations of regulatory T cells and their soluble products. The role of B cells in the regulation of CD4-dependent host responses is less well understood. Hepatic egg granuloma formation and fibrosis in murine schistosomiasis are dependent on CD4⁺ lymphocytes, and previous studies have implicated CD8⁺ T cells or cross-regulatory cytokines produced by T helper (Th) lymphocytes as controlling elements of this pathologic process. In this report, we demonstrate that B cell–deficient (μMT) mice exposed to Schistosoma mansoni develop augmented tissue pathology and, more importantly, fail to undergo the spontaneous downmodulation in disease normally observed during late stages of infection. Unexpectedly, B cell deficiency did not significantly alter T cell proliferative response or cause a shift in the Th1/Th2 balance. Since schistosome-infected Fc receptor–deficient (FcR γ chain knockout) mice display the same exacerbated egg pathology as that observed in infected μMT mice, the B cell– dependent regulatory mechanism revealed by these experiments appears to require receptor-mediated cell triggering. Together, the data demonstrate that humoral immune response/FcR interactions can play a major role in negatively controlling inflammatory disease induced by CD4⁺ T cells.     

Differential Effects of B Cell Receptor and B Cell Receptor–FcγRIIB1 Engagement on Docking of Csk to GTPase-activating Protein (GAP)-associated p62

The stimulatory and inhibitory pathways initiated by engagement of stimulatory receptors such as the B cell receptor for antigen (BCR) and inhibitory receptors such as Fcγ receptors of the IIB1 type (FcγRIIB1) intersect in ways that are poorly understood at the molecular level. Because the tyrosine kinase Csk is a potential negative regulator of lymphocyte activation, we examined the effects of BCR and FcγRIIB1 engagement on the binding of Csk to phosphotyrosine-containing proteins. Stimulation of a B lymphoma cell line, A20, with intact anti-IgG antibody induced a direct, SH2-mediated association between Csk and a 62-kD phosphotyrosine-containing protein that was identified as RasGTPase-activating protein–associated p62 (GAP-A.p62). In contrast, stimulation of A20 cells with anti-IgG F(ab′)₂ resulted in little increase in the association of Csk with GAP-A.p62. The effect of FcγRIIB1 engagement on this association was abolished by blockade of FcγRIIB1 with the monoclonal antibody 2.4G2. Furthermore, the increased association between Csk and GAP-A.p62 seen upon stimulation with intact anti-Ig was abrogated in the FcγRIIB1-deficient cell line IIA1.6 and recovered when FcγRIIB1 expression was restored by transfection. The differential effects of BCR and BCR-FcγRIIB1–mediated signaling on the phosphorylation of GAP-A.p62 and its association with Csk suggest that docking of Csk to GAP-A.p62 may function in the negative regulation of antigen receptor–mediated signals in B cells.     

A Cytokine–Cytokine Interaction in the Assembly of Higher-Order Structure and Activation of the Interleukine-3:Receptor Complex

Interleukine-3 (IL-3) binds its receptor and initiates a cascade of signaling processes that regulate the proliferation and differentiation of hematopoietic cells. To understand the detailed mechanisms of IL-3 induced receptor activation, we generated a homology model of the IL-3:receptor complex based on the closely related crystal structure of the GM-CSF:receptor complex. Model-predicted interactions between IL-3 and its receptor are in excellent agreement with mutagenesis data, which validate the model and establish a detailed view of IL-3:receptor interaction. The homology structure reveals an IL-3:IL-3 interaction interface in a higher-order complex modeled after the dodecamer of the GM-CSF:receptor complex wherein an analogous GM-CSF:GM-CSF interface is also identified. This interface is mediated by a proline-rich hydrophobic motif (PPLPLL) of the AA′ loop that is highly exposed in the structure of isolated IL-3. Various experimental data suggest that this motif is required for IL-3 function through receptor-binding independent mechanisms. These observations are consistent with structure-function studies of the GM-CSF:receptor complex showing that formation of the higher-order cytokine:receptor complex is required for signaling. However, a key question not answered from previous studies is how cytokine binding facilitates the assembly of the higher-order complex. Our studies here reveal a potential cytokine–cytokine interaction that participates in the assembly of the dodecamer complex, thus linking cytokine binding to receptor activation.     

Incorporation of Labeled Precursors into A16886B, a Novel β-Lactam Antibiotic Produced by Streptomyces clavuligerus

The incorporation of C-14 from amino acids into A16886B, 7-(5-amino-5-carboxyvaleramido)-7-methoxy-3-carbamoyloxymethyl-3-cephem-4- carboxylic acid, by Streptomyces clavuligerus is reported. As with cephalosporin C biosynthesis by the mold Cephalosporium acremonium, labels from cysteine, valine, and alpha-amino-adipic acid were incorporated. Unlike cephalosporin C, in A16886B label from lysine was incorporated into the alpha-aminoadipic acid side chain. Label from methionine-(14)C-methyl was incorporated into the methoxyl group. The relative percentage of incorporation of (3)H and (14)C from doubly labeled cystine suggests the improbability of the C-7 methoxyl group arising from an intermediate containing a double bond between C-6 and C-7.     

STRL33, A Novel Chemokine Receptor–like Protein, Functions as a Fusion Cofactor for Both Macrophage-tropic and T Cell Line–tropic HIV-1

The chemokine receptors CXCR4, CCR2B, CCR3, and CCR5 have recently been shown to serve along with CD4 as coreceptors for HIV-1. The tropisms of HIV-1 strains for subgroups of CD4⁺ cells can be explained, at least partly, by the selective use of G protein–coupled receptors (GPCRs). We have identified a novel human gene, STRL33, located on chromosome 3 that encodes a GPCR with sequence similarity to chemokine receptors and to chemokine receptor–like orphan receptors. STRL33 is expressed in lymphoid tissues and activated T cells, and is induced in activated peripheral blood lymphocytes. When transfected into nonhuman NIH 3T3 cells expressing human CD4, the STRL33 cDNA rendered these cells competent to fuse with cells expressing HIV-1 envelope glycoproteins (Envs). Of greatest interest, STRL33, in contrast with CXCR4 or CCR5, was able to function as a cofactor for fusion mediated by Envs from both T cell line–tropic and macrophage-tropic HIV-1 strains. STRL33-transfected Jurkat cell lines also supported enhanced productive infection with HIV-1 compared with control Jurkat cells. Despite the sequence similarities between STRL33 and chemokine receptors, STRL33-transfected cell lines did not respond to any in a panel of chemokines. Based on the pattern of tissue expression of the STRL33 mRNA, and given the ability of STRL33 to function with Envs of differing tropisms, STRL33 may play a role in the establishment and/or progression of HIV-1 infection.     

Core–shell silica–rhodamine B nanosphere for synthetic opals: from fluorescence spectral redistribution to sensing

Photonic crystals are a unique tool to modify the photoluminescence of light-emitting materials. A variety of optical effects have been demonstrated by infiltrating opaline structures with photoactive media. On the other hand, the fabrication of such structures includes complex infiltration steps, that often affect the opal lattice and decrease the efficiency of light emission control. In this work, silica nanospheres were directly functionalized with rhodamine B to create an emitting shell around the dielectric core. Simple tuning of the microsphere preparation conditions allows selecting the appropriate sphere diameter and polydispersity index approaching 5%. These characteristics allow facile self-assembling of the nanospheres into three-dimensional photonic crystals whose peculiar density of photonic states at the band-gap edges induces spectral redistribution of the rhodamine B photoluminescence. The possibility to employ the new stable structure as sensor is also investigated. As a proof of principle, we report the variation of light emission obtained by exposure of the opal to vapor of chlorobenzene.

Silica nanospheres were functionalized with rhodamine B and self-assembled into opals. Photoluminescence redistribution and pollutant responsivity were also investigated.     

Epitope-dependent Selection of Highly Restricted or Diverse T Cell Receptor Repertoires in Response to Persistent Infection by Epstein-Barr Virus

The T cell receptor (TCR) repertoires of cytotoxic responses to the immunodominant and subdominant HLA A11–restricted epitopes in the Epstein-Barr virus (EBV) nuclear antigen-4 were investigated in four healthy virus carriers. The response to the subdominant epitope (EBNA4 399-408, designated AVF) was highly restricted with conserved Vβ usage and identical length and amino acid motifs in the third complementarity-determining regions (CDR3), while a broad repertoire using different combinations of TCR-α/β V and J segments and CDR3 regions was selected by the immunodominant epitope (EBNA4 416-424, designated IVT). Distinct patterns of interaction with the A11–peptide complex were revealed for each AVF- or IVT-specific TCR clonotype by alanine scanning mutagenesis analysis. Blocking of cytotoxic function by antibodies specific for the CD8 coreceptor indicated that, while AVF-specific TCRs are of high affinity, the oligoclonal response to the IVT epitope includes both low- and high-affinity TCRs. Thus, comparison of the memory response to two epitopes derived from the same viral antigen and presented through the same MHC class I allele suggests that immunodominance may correlate with the capacity to maintain a broad TCR repertoire.Recognition of MHC–peptide complexes by TCRs is an essential step in the establishment of protective immunity (1). The TCR is a heterodimer composed of two polypeptide chains, α and β or γ and δ, which contain a variable domain, involved in antigen recognition, and a constant domain which is important for membrane attachment and T cell activation (2). The variable domain is encoded by multiple variable (V), diversity (D), and joining (J) gene segments. Somatic DNA rearrangement during lymphocyte differentiation in the thymus juxtapose V-J or V-D-J segments that code for the α/γ and β/δ chains, respectively. This combinatorial capacity creates an array of unique TCRs capable of recognizing a large variety of epitopes. The diversity is further increased by several possible α/β or γ/δ pairings and by nucleotide additions and/or trimming at the V(D)J junctions. The size of the repertoire that may potentially interact with a given antigen is narrowed by positive and negative selection in the thymus (3, 4). Further restrictions are imposed on the peripheral repertoire by the nature of the antigenic stimulus where the antigenic load and the persistence of the stimulus over a long period of time are likely to be important parameters (5).CTLs expressing the TCR-α/β–heterodimer and CD8 coreceptor play a critical role in controlling infection by EBV, a widespread human herpes virus that persists in healthy carriers as a latent infection of B cells (6, 7). In spite of the large complexity of the virus, which encodes for at least 9 proteins expressed in latently infected B lymphocytes, the CTL response detected during primary EBV infection appears to be preferentially focused on only few epitopes that are mainly derived from the high molecular weight Epstein-Barr virus nuclear antigens (EBNA)¹ 3, 4, and 6 (also known as EBNA 3A, 3B, and 3C) (8, 9). The reason for this strong focusing is presently unknown, but it is remarkable that a very similar hierarchy of epitope choice is maintained in the memory CTL responses that can be reactivated by in vitro stimulation of lymphocytes from healthy virus carriers. We have previously reported that EBV-specific CTL responses of HLA A11⁺ Caucasians are frequently dominated by A11-restricted CTLs that are directed to several epitopes derived from EBNA4 (10–12). The cognate peptides of two epitopes have been mapped within EBNA4 residues 416-424 (IVTDFSVIK, designated IVT) and 399-408 (AVFDRKSDAK, designated AVF) (11, 12). IVT-specific effectors may account for as much as 80% of the EBV-specific CTL clones isolated from these donors indicating that this is the immunodominant epitope (13). The immunodominance of the IVT epitope has recently been confirmed in a study that compared the frequency of specific CTL precursors in primary and memory response (14). Mutations affecting the anchor residues of the IVT peptide were shown to abrogate CTL recognition in EBV isolates from Southeast Asia, where HLA A11 is expressed in >50% of the population. Only half of the Southeast Asian isolates carried concomitant mutations within the AVF peptide, suggesting that CTL responses to IVT may exert a stronger selective pressure in vivo (12, 15). We have exploited these features to examine to what extent immunogenicity may affect the diversity of TCR repertoires specific for different viral epitopes during long-term persistent infection, where the opportunity for selection of T cell clones with maximal affinity might be optimal.     

A Receptor Mechanism for the Inhibition Of Insulin Release by Epinephrine in Man

Normal adult men and women have been infused with epinephrine, 6 mug per minute, during lipolytic blockade with nicotinic acid, beta-adrenergic blockade with propranolol and Butoxamine, and alpha-adrenergic blockade with phentolamine. Epinephrine infusion was associated with low serum levels of immunoreactive insulin (IRI) except when phentolamine was given simultaneously. These findings are compatible with an alpha receptor mechanism for the epinephrine inhibition of insulin release. Phentolamine had no blocking effects on the tachycardia and widened pulse pressure or lipolytic stimulation by epinephrine, whereas both propranolol and Butoxamine blocked lipolysis, tachycardia, and widened pulse pressure. These findings are consistent with an alpha receptor blocking action for phentolamine and beta receptor blocking action for propranolol and Butoxamine. Inhibition of lipolysis by nicotinic acid did not alter IRI or glucose responses to epinephrine. It is concluded that the lipolytic effect of epinephrine is unrelated to its effects on IRI release. Lipolytic blockade by nicotinic acid also did not change IRI or glucose in fasting subjects or their responses to a glucose infusion, 300 mg per minute. These observations appear to conflict with the Randle hypothesis (the glucose-fatty acid cycle) and raise some doubt as to whether plasma FFA concentrations are direct determinants of glucose or IRI concentrations in normal man.     

Assembly with copper(ii) ions and D–π–A molecules on a graphene surface for ultra-fast acetic acid sensing at room temperature

In this study, a graphene-based composite 4HQ-rGO/Cu²⁺ was prepared via the supramolecular assembly of graphene nanosheets with 4-hydroxyquinoline (4HQ) and copper(ii) ions. The as-prepared supramolecular assembly exhibited an excellent and enhanced sensing performance towards acetic acid at room-temperature, which was due to the fact that the D–π–A molecules, i.e. 4HQ, were able to accelerate the charge transfer between the graphene nanosheets and 4HQ molecules when acetic acid was attached. In addition, at room temperature, the copper(ii) ions also played a critical role as the main active site for gas adsorption, and thus the as-fabricated sensor exhibited a high response, outstanding selectivity, and ultra-fast response/recovery time. To examine the selectivity of the Cu²⁺ ions for the supramolecular assembly, various other transition metal ions such as Mn²⁺, Fe³⁺, Co²⁺, Ni²⁺, Cu²⁺, and Cd²⁺ were attached to the 4HQ-rGO assembly, and their acetic sensing performance was determined. Interestingly, the supramolecular assembly with the Cu²⁺ ions (4HQ-rGO/Cu²⁺) exhibited the best sensing performance compared to other metal ion-based 4HQ-rGO materials. Compared with the typical acetic acid gas sensors reported in the literature, it is noteworthy to mention that the as-prepared 4HQ-rGO/Cu²⁺ supramolecular assembly exhibited the shortest gas response time (within 5 s) at room temperature. The presented study demonstrates that the as-prepared supramolecular assembly is a promising material as a room temperature acetic acid gas sensor in practical applications.

The as-prepared 4HQ-rGO/Cu²⁺ sensor possessed a high response, outstanding selectivity and fast response-recovery characteristic, which was mainly attributed to the supramolecularly assemble of 4-hydroxyquinoline, and Cu²⁺ with graphene nanosheets.     

Novel green manufacture of metallic aluminum coatings on carbon steel by sol–gel method

Industrial processes for fabricating hot-dipping aluminum coatings on carbon steels involve problems related to equipment complexity, environmental issues and high energy consumption. To address these problems, a novel method for manufacturing metallic aluminum coating on carbon steel Q235 at room temperature by sol–gel method was developed in this work. Both the single-layer coating (47 μm) and the double-layer coating (97 μm) specimens were prepared by spraying some aqueous silica sol slurries containing spherical and flaky micro metallic aluminum powders on the steel surface at room temperature and then drying them at 50 °C. When the two coating specimens were heated at 500 °C for 10 h, heated double-layer specimens were thus obtained. It was found that the double-layer and the heated double-layer specimens didn''t rust at all after being soaked in aerated 3.5 wt% NaCl for 30 days. The shielding effect of the compact top coating was the main anticorrosion mechanism of the double-layer coating based on some electrochemical impedence spectroscopies and potentiodynamic polarization curves. Both coatings comprised only one metallic Al phase based on XRD. A very small quantity of Al₂O₃ phase appeared only after heating both coating specimens at 500 °C in the air for 10 h. In both cases the coatings didn''t crack at all after being heated at 500 °C in the air for 15 h by SEM observation and the oxidation rates of the steel substrates under these conditions were reduced by over 72% owing to the presence of the coatings. The average adhesive strengths of the single-layer and double-layer Al coatings were 12.06 MPa and 11.23 MPa, respectively, which were much larger than the corresponding value (max 8 MPa) of an ordinary anti-rusting epoxy coating on Q235 steel. Compared to the conventional hot-dipping aluminum or aluminized process, this novel method eliminates all the high temperature processes and thus saves a lot of energy, eliminates the use of all hazardous fluorides or chlorides and explosive H₂, avoids the formation of the voids inside aluminized coating, reduces the hot-dipped Al coating defects, can be applied for the steel plates with over 0.8 mm thickness, and can be applied in situ to repair damaged Al or Zn coatings.

The novel double-layer specimen of Al coating had the ability to resist simulated seawater corrosion for 30 days and air oxidation at 500 °C for 15 h.     

A Study of the Interferon Antiviral Mechanism: Apoptosis Activation by the 2–5A System

The 2–5A system contributes to the antiviral effect of interferons through the synthesis of 2–5A and its activation of the ribonuclease, RNase L. RNase L degrades viral and cellular RNA after activation by unique, 2′–5′ phosphodiester-linked, oligoadenylates [2–5A, (pp)p5′ A2′(P5′A2′)]_n, n 2. Because both the 2–5A system and apoptosis can serve as viral defense mechanisms and RNA degradation occurs during both processes, we investigated the potential role of RNase L in apoptosis. Overexpression of human RNase L by an inducible promoter in NIH3T3 fibroblasts decreased cell viability and triggered apoptosis. Activation of endogenous RNase L, specifically with 2–5A or with dsRNA, induced apoptosis. Inhibition of RNase L with a dominant negative mutant suppressed poly (I)·poly (C)–induced apoptosis in interferon-primed fibroblasts. Moreover, inhibition of RNase L suppressed apoptosis induced by poliovirus. Thus, increased RNase L levels induced apoptosis and inhibition of RNase L activity blocked viral-induced apoptosis. Apoptosis may be one of the antiviral mechanisms regulated by the 2–5A system.     

Mast Cell Granule-Mediated Uptake of Low Density Lipoproteins by Macrophages: A Novel Carrier Mechanism Leading to the Formation of Foam Cells

Mast cells are present in the arterial intima, the site of atherogenesis. To gain insight into the possible role of mast cells in the formation of the cholesterol-loaded macrophage foam cells typical of both early and late atherosclerotic lesions, a model system was developed in which isolated rat serosal mast cells were incubated with mouse peritoneal macrophages in medium to which low-density lipoproteins (LDL) had been added. Stimulation of the mast cells was found to induce a 50-fold enhancement of LDL uptake by the macrophages, which concomitantly accumulated LDL-derived cholesterol. This process, called the “granule-mediated uptake of LDL”, involves the following steps: (i) exocytosis of the cytoplasmic granules of the mast cells, (ii) escape of soluble granule components, such as histamine and a fraction of the granule heparin proteoglycans into the medium, leaving granule remnants consisting of neutral proteases embedded in a heparin proteoglycan matrix, (iii) binding of LDL to binding sites on the glycosaminoglycan side chains of the heparin proteoglycan component of the granule remnants, (iv) proteolytic degradation of the bound LDL by the neutral proteases of the granule remnants, (v) fusion of degraded LDL particles on the surfaces of the granule remnants, and (vi) phagocytosis of the LDL-laden granule remnants by the macrophages. Simultaneously, the soluble heparin proteoglycans, to which no proteolytic enzymes are bound, interact with LDL with formation of insoluble complexes which are also phagocytosed by the macrophages. Finally, cholesterol derived from the granule remnant-bound LDL and the LDL-heparin proteoglycan complexes becomes esterified by the macrophages, with formation of macrophage foam cells. Experiments in vivo showed that granule remnants may also carry LDL into macrophages in the peritoneal cavity of the rat, where mast cells and macrophages coexist. The results suggest that mast cells play an active role in the intracellular cholesteryl ester deposition characteristic of human atherosclerotic lesions.     

NKG2D-MICA/B在急性白血病免疫逃逸机制中的作用

目的探讨NK细胞活化性受体（NKG2D）-MICA/B在急性白血病肿瘤免疫逃逸机制中的作用。方法选择20例初发未治疗的急性白血病患者,应用流式细胞术检测白血病细胞表面MICA/B表达水平、ELISA法检测血清可溶性MICA及MICB（sMICA,sMICB）水平,同时检测患者NKG2D表达水平。选择5例健康人做为对照。结果（1）20例急性白血病患者白血病细胞表面不表达或弱表达MICA/B,正常人淋巴细胞表面不表达MICA/B。（2）患者血清sMICA和sMICB水平均高于对照组,差异有统计学意义（P〈0.01）。（3）患者NKG2D表达水平低于对照组,差异有统计学意义（P〈0.01）。结论白血病细胞表面MICA和MICB的脱落损伤基于NKG2D-MIC的抗白血病效应,可能是导致急性白血病免疫逃逸的机制之一。     

Effect of fluorine substituents on benzothiadiazole-based D–π–A′–π–A photosensitizers for dye-sensitized solar cells

Two D–π–A′–π–A organic dyes with triazatruxene (TAT) as the electron donor, thiophene as the π-spacer, benzoic acid as the anchor group, and benzothiadiazole (BT) or difluorobenzo[c][1,2,5]thiadiazole (DFBT) as the additional acceptor, namely LS101 and LS102, respectively, were applied to dye-sensitized solar cells (DSSCs). As fluorine substituents are usually strong electron-withdrawing groups, introducing two fluorine atoms into BT was expected to strengthen the electron-withdrawing ability of the auxiliary acceptor, resulting in DSSCs with a broader light capture region and further improved power conversion efficiency (PCE). Fluorine is the smallest electron-withdrawing group with an induction effect, but can also act as an electron-donating group owing to its conjugation effect. When the conjugation effect is dominant, the electron-withdrawing ability of additional acceptor DFBT decreases instead. Accordingly, the band gap of LS102 was broadened and the UV-vis absorption spectrum was blue-shifted. In the end, DSSCs based on LS101 achieved a champion PCE of 10.2% (J_sc = 15.1 mA cm⁻², V_oc = 966 mV, FF = 70.1%) while that based on LS102 gave a PCE of only 8.6% (J_sc = 13.4 mA cm⁻², V_oc = 934 mV, FF = 69.1%) under standard AM 1.5G solar irradiation (100 mW cm⁻²) with Co²⁺/Co³⁺ as the electrolyte.

The results and interpretations can clearly explain the reasons for the poor photovoltaic performance of DFBT in DSSCs.