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Metasurfaces are artificial materials that can provide properties not readily available in nature for the interaction with acoustic, elastodynamic, or electromagnetic waves. In Electromagnetics, metasurfaces allow particular functionalities to antennas, which in turn lately have been increasingly pushed to a multiband operation. To fully exploit metasurfaces' capabilities, the use of a metasurface reflector and a metasurface superstrate surrounding a radiating element in multiband antennas is interesting. However, such topology generally creates multiple reflections inside the formed cavity, known as Fabry-Pérot resonances. Here we show that one should tame this phenomenon to use two parallel metasurfaces surrounding a planar radiating element. We present the conditions to obtain directive, multiband antennas under such circumstances. The concepts are validated with a compact device for 5G/4G/Wi-Fi 2.4/5/6E performing a beam steering in the 5G without disturbing the radiation patterns of the other bands. This device demonstrates that the functionalities of two metasurfaces may be exploited in a single design if the presented conditions are respected. We also anticipate our work to be a starting point for other studies in the wave domain. For example, compact, multiband, beam-steerable microphones or sonar transducers with two parallel metasurfaces could be investigated in the future., (© 2023. The Author(s).)

When a wideband antenna is backed by an artificial magnetic conductor (AMC) reflector, the bandwidth is reduced. With the optimization of the shape of the AMC it is possible to exhibit multiband behavior, but the problem becomes complex if the bands are also intended to be wide. In this study, a methodology that exploits both the expected in-band and out-of-band behaviors of a dual-band AMC was used to design a low-profile, triple-band, and wideband directive antenna. The methodology was validated with a prototype suitable for the European standards of 4G/5G and Wi-Fi 2.4/5/6E, operating within the following bands: 2.4-2.7 GHz, 3.4-3.8 GHz, and 5.17-6.45 GHz. The measured results showed respective peak values of 8.0, 9.1, and 10.5 dBi for the broadside realized gain, front-to-back ratios larger than 19 dB, cross-polarized levels lower than -18 dB, and stable half-power beamwidths within each band. Furthermore, 3 dB gain bandwidths of 34.4%, 19.7%, and 31.0% were also measured.

In order to extend the performance of radar absorbing materials, it is necessary to design new structures with wideband properties and large angles of incidence which are also as thin as possible. The objective of this work, realized within the framework of the SAFAS project (self-complementary surface with low signature) is, then, the development of an ultra-wideband microwave absorber of low thickness. The design of such material requires a multilayered structure composed with dielectric layers, metasurfaces, and wide-angle impedance matching layers. This solution has been realized with on-the-shelf materials, and measured to validate the concept. At normal incidence, the bandwidth ratio, defined for a magnitude of the reflection coefficient below -10 dB, is 4.7:1 for an absorber with a total thickness of 11.5 mm, which corresponds to λ/7 at the lowest operating frequency. For an incidence of 60°, this bandwidth ratio is reduced to 3.8:1, but the device remains ultra-wideband.

Background & Aims: Acute inflammatory ileitis occurs in susceptible (C57BL/6) mice after oral infection with Toxoplasma gondii. Overproduction of interferon (IFN)-gamma and synthesis of nitric oxide mediate the inflammation. We evaluated the role of transforming growth factor (TGF)-beta produced by intraepithelial lymphocytes (IELs) in this process., Methods: We analyzed the histologic and immunologic consequences of adoptive transfer of antigen-primed IELs into susceptible mice treated with anti-TGF-beta before oral challenge with T. gondii cysts. An in vitro coculture of enterocytes and IELs assessed the production of chemokines and cytokines in the presence of anti-TGF-beta., Results: Antigen-primed IELs prevent acute ileitis in susceptible mice that is reversed with anti-TGF-beta. Resistant mice (CBA/J) develop ileitis after treatment with anti-TGF-beta. Antigen-primed IELs can induce systemic immunosuppression as measured by depressed IFN-gamma production. In vitro, primed IELs reduce the production of inflammatory chemokines by infected enterocytes and IFN-gamma by splenocytes., Conclusions: Regulation of the ileal inflammatory process resulting from T. gondii is dependent on TGF-beta-producing IELs. The IELs are an essential component in gut homeostasis after oral infection with this parasite.

Intranasal (i.n.) immunization with the SAG1 protein of Toxoplasma gondii plus cholera toxin (CT) provides protective immunity. The aim of this study was to analyze the cellular activation of several mucosal compartments after i.n. immunization. Cervical and mesenteric lymph node (CLN and MLN, respectively) lymphoid cell and intraepithelial lymphocyte (IEL) passive transfer experiments were performed with CBA/J mice immunized i.n. with SAG1 plus CT. CLN and MLN cells and IEL isolated 42 days after immunization conferred protective immunity on naive recipient mice challenged with strain 76K T. gondii, as assessed by the reduction in the number of brain cysts. There were proliferative specific responses in nose-associated lymphoid tissue and the CLN and MLN cells from mice immunized with SAG1 plus CT, but no cytokine was detectable. Thus, protective immunity is associated with a specific cellular response in the nasal and mesenteric compartments after i.n. immunization.

Toxoplasma gondii Ag-primed intraepithelial lymphocytes (IEL) from the mouse intestine have been shown to be protective against an lethal parasite challenge when adoptively transferred into recipient mice. In the present study, we observed that Ag-primed IEL traffic to the intestine of naive mice following i.v. administration. Primed and CD8beta+ IEL were the most efficient cells at homing to the host organ. In congenic mice, IEL migrated from intestine within several hours posttransfer. On Ag reexposure, the primed IEL return to the intestine where they enhance resistance as determined by reduction in the number of brain cysts. Treatment of recipient mice with anti-alpha4 and anti-alphaE Abs partially inhibited IEL intestinal homing. The Ab treatment dramatically impaired resistance to a subsequent oral infection. These finding indicate that lymphocyte homing is an important parameter in establishing long term immunity to recurrent infection with this parasite.

We have developed a murine model to investigate the pathogenesis of acquired ocular toxoplasmosis. Tachyzoites of PLK strain of Toxoplasma gondii were intracamerally inoculated under anesthesia into the right eyes of naive or perorally preinfected C57BL/6 and MRL-MpJ mice. Clinical and histopathological observations of responses to intraocular infection were analyzed. Ocular inflammation from Toxoplasma gondii is dose-dependent in both strains of mice. After inoculation of fifty parasites, no evidence of inflammation was observed in the eyes of naive mice. The eyes of naive mice that received 500 or 5,000 parasites developed inflammatory changes by day 6 post challenge. By day 8, the changes progressed to moderate to severe intraocular inflammation. Histologic analysis of the ocular lesions demonstrated mononuclear cell infiltration and necrosis predominantly in the anterior segment of the eyes of the naive mice. Inoculation of 50,000 tachyzoites induced a destructive ocular inflammatory response and was uniformly lethal to the mice by approximately one week after challenge. In contrast, eyes from mice previously orally infected with Toxoplasma gondii and that received a 50 or 500 parasite intracameral challenge revealed no inflammation, but the eyes receiving 5,000 parasites demonstrated necrotic focal retinochoroiditis with vitreitis by day 8 after challenge. The murine model reproduces some features of ocular toxoplasmosis in humans and may be suitable for large-scale controlled studies of the pathogenesis and therapeutics of acquired ocular toxoplasmosis as well as for study of the mechanisms of immune privilege in the eye.

Intraepithelial lymphocytes (IEL) of the intestine represent an important barrier in the prevention of infection against orally acquired pathogens. Adoptive transfer of Ag-primed IEL into a naive host can protect against challenge. Using a murine model, we demonstrate in two genetically distinct mouse strains (C57BL/6 and CBA/J) that protective IEL can be isolated at specific times after oral infection with cysts containing bradyzoites. Adoptive transfer of IEL obtained from the intestine of infected mice at these specific times can provide long term protection, as determined by mortality and cyst number against challenge. The protective IEL appear to be CD8+, TCR-alpha/beta and are at least partially dependent upon the presence of TCR-gamma/delta T cells in the host. Endogenous production of the pivotal cytokine, IFN-gamma, is essential for host immunity. These findings demonstrate that gut-derived IEL represent a potentially important mechanism to provide long term immunity to the host.

Intraepithelial lymphocytes (IEL) of the gut represent a primary immune barrier against infection by orally acquired pathogens. Naturally acquired infection with Toxoplasma gondii induces the proliferation of CD8+ T cells in both the gut and spleen. Gut-derived CD8alpha/beta+ IEL exhibit MHC-restricted cytotoxicity against parasite-infected enterocytes and macrophages. In a murine model, we demonstrate that the adoptive transfer of IEL obtained from inbred mice at day 11 postinfection is able to protect against a virulent challenge in syngenic recipients. In CBA mice, the parasite cyst load within the brain of the recipients receiving primed IEL was reduced by 90%. In BALB/c and C57BL/6 mice, a 50% decrease in mortality was observed following adoptive transfer of primed IEL. To determine the T cell subset responsible for protective immunity, a purified CD8alpha/beta+ IEL population was isolated from infected mice at day 11 postinfection. These cells were able to protect naive mice by adoptive transfer against a lethal parasite challenge. RNA analysis by reverse-transcriptase PCR revealed that primed CD8alpha/beta+ IEL produce significant message for IFN-gamma, an essential cytokine for host protection against toxoplasmosis. Administration of anti-IFN-gamma at the time of adoptive transfer of primed IEL abrogated protection. The adoptive transfer of these protective IEL was not restricted to the Ld class I locus. These data demonstrate that IFN-gamma-producing IEL may be an important primary barrier against acute and perhaps recurrent infection with T. gondii.